Antioxidant and methyl donor effects of betaine versus ethanol-induced oxidative stress in the rat liver

Oxidative stress is one hypothesis for the association of ethanol consumption with cardiovascular, cerebrovascular, and liver diseases. Thus, we examined whether oral betaine can act as a preventive agent in ethanol-induced oxidative stress on the rat liver. A total of 32 male Sprague–Dawley rats were divided into four equal groups. The control group received normal saline. The ethanol group was administered ethanol (4 g/kg). The betaine group received betaine [1.5 % (w/w) of the total diet], and the betaine plus ethanol group (Bet. & Eth.) were administered with betaine; after 120 min, the rats received ethanol. All of the treatments were applied for 2 months via gavage. Elevation of glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were observed in the betaine-treated groups. Thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation) concentration also decreased in the betaine-treated rats as compared to the ethanol group. There was also a significant reduction in plasma total homocysteine (tHcy) concentration in the betaine and Bet. & Eth. groups as compared to the ethanol-treated rats. In contrast, ethanol treatment in rats resulted in significant lower antioxidant enzyme activities (GPx and SOD), and indicated lipid peroxidation to the liver, as monitored by the elevation in TBARS level. Administration of ethanol to rats also induced toxicity in their liver, as shown by the histopathological findings, whereas betaine could suppress liver damages in the Bet. & Eth. group. Overall, oral pretreatment with betaine significantly prevented ethanol-induced oxidative stress and hyperhomocysteinemia via increasing antioxidant enzyme activities and decreasing tHcy concentration. Thus, betaine may be recommended as a therapeutic agent for patients with liver damages induced by oxidative stress in various diseases.     

Oleuropein attenuates cognitive dysfunction and oxidative stress induced by some anesthetic drugs in the hippocampal area of rats

The present study was designed to evaluate the antioxidant effects of oleuropein against oxidative stress in the hippocampal area of rats. We used seven experimental groups as follows: Control, Propofol, Propofol-Ketamine (Pro.-Ket.), Xylazine-Ketamine (Xyl.-Ket.), and three oleuropein-pretreated groups (Ole.-Pro., Ole.-Pro.-Ket. and Ole.-Xyl.-Ket.). The oleuropein-pretreated groups received oleuropein (15 mg/kg body weight as orally) for 10 consecutive days. Propofol 100 mg/kg, xylazine 3 mg/kg, and ketamine 75 mg/kg once as ip was used on the 11th day of treatment. Spatial memory impairment and antioxidant status of hippocampus were measured via Morris water maze, lipid peroxidation marker, and antioxidant enzyme activities. Spatial memory impairment and lipid peroxidation significantly increased in Xyl.-Ket.-treated rats in comparison to the control, propofol, Ole.-Pro. and Ole.-Pro.-Ket. groups. Oleuropein pretreatment significantly reversed spatial memory impairment and lipid peroxidation in the Ole.-Xyl.-Ket. group as compared to the Xyl.-Ket.-treated rats. There was no significant difference between the control and the propofol group in lipid peroxidation and spatial memory status. Superoxide dismutase and catalase activities both significantly decreased in Xyl.-Ket.-treated rats when compared to the control, propofol, Ole.-Pro., Ole.-Pro.-Ket., and Ole.-Xyl.-Ket. groups. In contrast, glutathione peroxidase activity in Xyl.-Ket.-treated rats significantly increased as compared to the control, propofol, Pro.-Ket., Ole.-Pro., and Ole.-Pro.-Ket. groups. We concluded that xylazine in combination with ketamine is an oxidative anesthetic drug and oleuropein pretreatment attenuates cognitive dysfunction and oxidative stress induced by anesthesia in the hippocampal area of rats. We also confirmed the antioxidant properties of propofol as a promising antioxidant anesthetic agent.     

Protective effect of Launaea procumbens (L.) on lungs against CCl

ABSTRACT: BACKGROUND: Launaea procumbens (L.) is traditionally used in the treatment of various human ailments including pulmonary damages. The present study was arranged to evaluate the role of Launaea procumbens methanol extract (LME) against carbon tetrachloride (CCl4) induced oxidative pulmonary damages in rat. METHODS: 36 Sprague--Dawley male rats (170-180 g) were randomly divided into 06 groups. After a week of acclamization, group I was remained untreated while group II was given olive oil intraperitoneally (i.p.) and dimethyl sulfoxide (DMSO) orally, groups III, IV, V and VI were administered CCl4, 3 ml/kg body weight (30% in olive oil i.p.). Groups IV, V were treated with 100 mg/kg, 200 mg/kg of LME whereas group VI was administered with 50 mg/kg body weight of rutin (RT) after 48 h of CCl4 treatment for four weeks. Antioxidant profile in lungs were evaluated by estimating the activities of antioxidant enzymes; catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), glutathione-S-transferase (GST), glutathione reductase (GSR), glutathione peroxidase (GSH-Px), quinone reductase (QR) and reduced glutathione (GSH). CCl4-induced lipid peroxidation was determined by measuring the level of thiobarbituric acid reactive substances (TBARS) with conjugation of deoxyribonucleic acid (DNA) damages, argyrophilic nucleolar organizer regions (AgNORs) counts and histopathology. RESULTS: Administration of CCl4 for 6 weeks significantly (p < 0.01) reduced the activities of antioxidant enzymes and GSH concentration while increased TBARS contents and DNA damages in lung samples. Co-treatment of LME and rutin restored the activities of antioxidant enzymes and GSH contents. Changes in TBARS concentration and DNA fragmentation were significantly (p < 0.01) decreased with the treatment of LME and rutin in lung. Changes induced with CCl4 in histopathology of lungs were significantly reduced with co-treatment of LME and rutin. CONCLUSION: Results of present study revealed that LME could protect the lung tissues against CCl4-induced oxidative stress possibly by improving the antioxidant defence system.     

<Emphasis Type="Italic">Tetracarpidium conophorum</Emphasis> ameliorates oxidative reproductive toxicity induced by ethanol in male rats

Background

Tetracarpidium conophorum (Mull. Arg.) Hutch. & Dalz is one of the many medicinal plants used for ages in folklore as male fertility enhancers. The current study evaluates the effect of the plant leaf extract on alcohol - induced reproductive toxicity in male rats.

Methods

Thirty rats were randomly divided into six groups of five animals each; Group 1 (positive control) received normal saline only; Group 2 (ethanol alone) were given only 30 % ethanol orally at 7 ml/kg body weight per day, thrice in a week; Group 3, 4, 5 were given ethanol and co-treated with 50 mg/kg, 500 mg/kg and 1000 mg/kg body weight of leaf extract respectively while Group 6 were given ethanol and co-treated with a fertility drug, clomiphene citrate. All the drugs were given daily and the experiment lasted for twenty one consecutive days.

Results

Alcohol ingestion resulted in a significant (p?<?0.05) decrease in water, food intake and marked elevation of lipid peroxidation as assessed by the accumulation of malondialdehyde (MDA) in the reproductive tissues. Precisely, MDA level was elevated in the testis, epididymis, seminal vesicle and prostate gland by 81 %, 63 %, 95 % and 91 %, respectively. Furthermore, levels of total protein, reduced glutathione (GSH), vitamin C and activities of antioxidant enzymes in the reproductive tissues were significantly (p?<?0.0001) reduced in ethanol-ingested rats. Interestingly, co-administration of T. conophorum with ethanol led to almost complete inhibition of lipid peroxidation thereby enhancing antioxidant status of the reproductive tissues.

Conclusion

Overall, T. conophorum ameliorates oxidative reproductive toxicity induced by ethanol in male rats and its ameliorative effect comparable well with the fertility drug, clomiphene citrate.

     

Neuroprotective effects of tramadol on cerebral injuries caused by hind limb ischaemia/reperfusion in rats

Skeletal muscle ischaemia–reperfusion-induced acute remote injury is mediated by activated neutrophils and formation of free radicals. Several investigators have demonstrated that the opioid pathway is involved in tissue preservation during hypoxia or ischaemia. Tramadol hydrochloride is an effective analgesic used for severe acute and chronic pain conditions. The present study was designed to investigate the potential protective effects of tramadol hydrochloride on cerebral oxidative stress and damage as well as lipid peroxidation, brain oedema and histological changes induced by hind limb ischaemia and reperfusion injury in rats. Thirty-six male Wistar rats were randomly allocated into two experimental groups: ischaemia–reperfusion (group I) and ischaemia–reperfusion + tramadol hydrochloride (group II). Hind limb ischaemia was induced by clamping the femoral artery. After 2-h ischaemia, the clamp from the femoral vessels was removed and the animal underwent 24-h reperfusion. Tramadol hydrochloride was given intravenously at a dose of 20 mg/kg, immediately before reperfusion. After reperfusion, animals were euthanized and the cerebral structure, lipid peroxidation and brain oedema in the cerebral tissue were assessed. Histopathological assessment of cerebral injury was split into four grades. The extent of lipid peroxidation was measured by estimating the amount of malondialdehyde. Brain oedema was calculated as the percentage water content of the brain. Brain oxidative stress and damage were significantly attenuated by treatment with tramadol hydrochloride. Compared with the ischaemia–reperfusion group, histological changes in brain tissues (p?p?P?相似文献   

Incretin attenuates diabetes-induced damage in rat cardiac tissue

Glucagon-like peptide-1 (GLP-1), as a member of the incretin family, has a role in glucose homeostasis, its receptors distributed throughout the body, including the heart. The aim was to investigate cardiac lesions following diabetes induction, and the potential effect of GLP-1 on this type of lesions and the molecular mechanism driving this activity. Adult male rats were classified into: normal, diabetic, 4-week high-dose exenatide-treated diabetic rats, 4-week low-dose exenatide-treated diabetic rats, and 1-week exenatide-treated diabetic rats. The following parameters were measured: in blood: glucose, insulin, lactate dehydrogenase (LDH), total creatine kinase (CK), creatine kinase MB isoenzyme (CK-MB), and CK-MB relative index; in cardiac tissue: lipid peroxide (LPO) and some antioxidant enzymes. The untreated diabetic group displayed significant increases in blood level of glucose, LDH, and CK-MB, and cardiac tissue LPO, and a significant decrease in cardiac tissue antioxidant enzymes. GLP-1 supplementation in diabetic rats definitely decreased the hyperglycemia and abolished the detrimental effects of diabetes on the cardiac tissue. The effect of GLP-1 on blood glucose and on the heart also appeared after a short supplementation period (1 week). It can be concluded that GLP-1 has beneficial effects on diabetes-induced oxidative cardiac tissue damage, most probably via its antioxidant effect directly acting on cardiac tissue and independent of its hypoglycemic effect.     

Methionine-supplemented diet augments hepatotoxicity and prooxidant status in chronically ethanol-treated rats

The purpose of this study was to investigate whether high methionine (HM) diet may influence the development of ethanol-induced hepatotoxicity and prooxidant–antioxidant balance in the liver. Rats received drinking water containing ethanol (20% v/v) and/or methionine supplemented diet (2% w/w) for 75 days. Although prooxidant–antioxidant balance did not change in the liver of rats in HM group, ethanol treatment was observed to increase plasma transaminase activities, and malondialdehyde (MDA) and protein carbonyl (PC) levels, but not glutathione (GSH), vitamin E and vitamin C levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver of rats as compared to controls. However, ethanol plus HM diet caused further increases in plasma transaminase activities and hepatic MDA and PC levels. In addition, SOD, GSH-Px and GST activities were observed to decrease, but GSH, vitamin E and vitamin C levels remained unchanged in the liver as compared to ethanol, HM and control groups. Our results show that HM diet may augment hepatotoxicity and oxidative stress in the liver of chronically ethanol-treated rats.     

<Emphasis Type="Italic">Biebersteinia multifida</Emphasis> DC a potential savior against testicular torsion-induced reperfusion injury

The study aimed to investigate the potential therapeutic effect of the methanolic extract of Biebersteinia multifida DC on ischemia–reperfusion injury induced by testicular torsion/detorsion in rats. Forty adult male Sprague-Dawley rats were randomly divided into four groups. Sham operation group, torsion/detorsion group plus saline, and torsion/detorsion groups plus 75 and 150 mg/kg doses of DC extract (administered intraperitoneally 15 min before detorsion). Testicular ischemia was induced via keeping the left testis under 720° counterclockwise torsion for 2 h; afterwards, detorsion was performed. All rats were sacrificed 4 h after detorsion and bilateral testes were removed for histological examinations. The testes in sham operation group had normal structure. Contralateral testicular tissue had mild injury in torsion/detorsion (T/D) group, while it was approximately normal in DC-treated group. In the T/D group, most of the testes demonstrated severe lesions in ipsilateral testes. In contrast, ipsilateral twisted testicular tissue in DC-treated group showed mild to moderate injuries. Similar histopathological results were obtained in both utilized therapeutic doses of DC (75 and 150 mg/kg). B. multifida is a rich source of phenolic antioxidant components that can be potentially used as a free radical scavenger in testicular damages caused by reperfusion injury, although more detailed studies are warranted.     

Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection

Oxidative stress is a disturbance in the oxidant-antioxidant balance leading to potential cellular damage. Most cells can tolerate a mild degree of oxidative stress because they have a system that counteracts oxidation that includes antioxidant molecules such as glutathione (GSH) and superoxide dismutase (SOD). Disruption of the host antioxidant status has been recognized as an important contributor to the pathogenesis of many viruses. Caraparu virus (CARV) is a member of group C of the Bunyaviridae family of viruses. In South American countries, group C bunyaviruses are among the common agents of human febrile illness and have caused multiple notable outbreaks of human disease in recent decades; nevertheless, little is known about the pathogenic characteristics of these viruses. The purpose of this study was to examine the hepatic pathogenesis of CARV in mice and the involvement of oxidative stress and antioxidant defenses on this pathology. Following subcutaneous infection of BALB/c mice, CARV was detected in the liver, and histopathology revealed acute hepatitis. Increased serum levels of aspartate and alanine aminotransferases (AST/ALT) and greater hepatic expression of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) were found in infected animals. CARV infection did not alter the biomarkers of oxidative stress but caused an increase in GSH content and altered the expression and activity of SOD. This is the first report of an alteration of oxidative homeostasis upon CARV infection, which may, in part, explain the hepatic pathogenesis of this virus, as well as the pathogenesis of other Bunyaviridae members.     

Red wine antioxidants protect hippocampal neurons against ethanol-induced damage: a biochemical, morphological and behavioral study

Chronic ethanol consumption increases oxidative stress, which accounts for the striking neurological changes seen in this condition. Notwithstanding, there is well-documented evidence that polyphenols, present in grape skin and seeds, exhibit a strong antioxidant activity. As red wine is rich in polyphenols, the aim of the present work was to evaluate their putative protective effects on the hippocampal formation by applying biochemical, morphological and behavioral approaches. Six-month old male Wistar rats were fed with red wine (ethanol content adjusted to 20%) and the results were compared with those from ethanol-treated (20%) rats and pair-fed controls. Biochemical markers of oxidative stress (lipid peroxidation, glutathione levels and antioxidant enzyme activities) were assessed on hippocampal homogenates. Lipofuscin pigment, an end product of lipid peroxidation, was quantified in hippocampal cornu ammonis 1 and 3 (CA1 and CA3) pyramidal neurons using stereological methods. All animals were behaviorally tested on the Morris water maze in order to assess their spatial learning and memory skills. In red wine-treated rats, lipid peroxidation was the lowest while presenting the highest levels of reduced glutathione and an induction of antioxidant enzyme activities. Morphological findings revealed that, contrary to ethanol, red wine did not increase lipofuscin deposition in CA1 and CA3 pyramidal neurons. Besides, red wine-treated animals learned the water maze task at a higher rate than ethanol group and had better performance scores by the end of the training period and on a probe trial. Actually, no significant differences were found between pair-fed controls and red wine-treated rats in morphological and behavioral data. Thus, our findings demonstrate that chronic consumption of red wine, unlike the ethanol solution alone, does not lead to a decline in hippocampal-dependent spatial memory. This may be due to the ability of red wine polyphenols to improve the antioxidant status in the brain and to prevent free radical-induced neuronal damage.     

Effect of <Emphasis Type="Italic">Cannabis sativa</Emphasis> extract on gastric acid secretion,oxidative stress and gastric mucosal integrity in rats

Studies were conducted in pylorus-ligated rats to investigate the effect of Cannabis sativa extract on gastric acid secretion, experimental gastric ulcer and on oxidative stress and inflammatory markers in the gastric mucosa. C. sativa (5, 10 and 20 mg/kg, expressed as Δ⁹-tetrahydrocannabinol) was administered subcutaneously daily for 4 weeks prior to pylorus ligation and different treatments. Under basal conditions, pretreatment with cannabis extract at doses of 5 and 10 mg/kg increased gastric acid secretion and induced minimally visible gastric mucosal lesions in the 4 h pylorus-ligated rat. Malondialdehyde and nitric acid concentration increased, while reduced glutathione decreased by cannabis at doses of 5 and 10 mg/kg in gastric mucosa. TNF-α increased by cannabis extract at doses of 5 and 10 mg/kg but decreased following the high dose of 20 mg/kg. On the other hand, the gastric acid secretory responses stimulated by pentagastrin or carbachol (but not histamine) were inhibited in rats pretreated with cannabis extract. Under these conditions, cannabis decreased pepsin content after pentagastrin and carbachol but not histamine stimulation. Cannabis also decreased lipid peroxidation and nitric oxide content, and increased both reduced glutathione and catalase activity in mucosa. Moreover, cannabis decreased mucosal inflammation (level of TNF-α) and the development of gastric mucosal lesions. Cannabis administered for 1 month prior to pylorus-ligation and either acidified aspirin or ethanol (96 %) decreased the development of gastric mucosal damage in a dose-dependent manner, along with reduction in gastric acid output, gastric mucosal oxidative stress and inflammation (TNF-α). Sections of gastric mucosa stained with periodic acid Schiff showed increased mucus secretion by cannabis in basal conditions and after treatment with aspirin or ethanol. Results indicate that: (1) the effect of cannabis differs in basal conditions and after exposure of the gastric mucosa to high acid concentrations or other chemical noxious agents; (2) cannabis administered systemically exerts gastric mucosal protective effects against mucosal damage evoked by stimulation of gastric acid secretion, acidified aspirin or ethanol. These effects of cannabis are likely to involve inhibition of gastric acid and pepsin secretion, increased mucus, decreased oxidative stress and inflammation in gastric mucosa.     

Preventive Effect of Chrysin on Bleomycin-Induced Lung Fibrosis in Rats

The aim of the current study is determination of protective effect of chrysin (CRS), a natural flavonoid, on cell injury produced by lung fibrosis induced with bleomycin (BLC) in rats. Twenty-eight female rats were assigned to four groups as follows: control group, CRS group; 50 mg/kg CRS was continued orally for 14 days, BLC group; a single intratracheal injection of BLC (2.5 mg/kg body weight in 0.25 ml phosphate buffered saline), BLC?+?CRS group; 50 mg/kg CRS was administered 1 day before the intratracheal BLC injection and continued for 14 days orally. All animals were sacrificed at day 14th after BLC administration. The semiquantitative assessment of histopathological consisting of lung inflammation and collagen deposition, tissue levels of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reducted glutathione (GSH) were measured. BLC provoked histological changes consisting of alveolar congestion, increase connective tissue, infiltration, and the thickness of alveolar wall were detected significantly when compared to the control group (p?≤?0.0001). CRS supplementation significantly restored these histological damages (p?≤?0.0001). The level of tissue TBARS was increased with BLC (p?GPx, CAT, and GSH in the lung tissue compared to control group (p?p?相似文献   

Antihyperlipidemic and antiinflammatory effect of Bhallataka nuts in ameliorating the alterations in lipid metabolism and inflammation in diabetes-induced cardiac damage in rats

Semecarpus anacardium Linn., which belongs to the Anacardiaceae family, has been used in both Ayurveda and Siddha system against various ailments. The present study was carried out to establish the antihyperlipidemic and antiinflammatory effect of S. anacardium Linn. nut milk extract (SA) in diabetes-induced cardiovascular complications in rats. Type 2 diabetes was induced in rats by feeding them with a high-fat diet for 2 weeks followed by intraperitoneal injection of streptozotocin (STZ) 35 mg/kg body wt twice 24 h apart dissolved in olive oil and left for 12 weeks to develop cardiovascular complication. High-fat diet and STZ induction significantly (p?相似文献   

Lipophilic copper(II) formulations: Some correlations between their composition and anti-inflammatory/anti-arthritic activity when applied to the skin of rats

Copper complexes of phenols related to salicylic acid were prepared in DMSO and applied to the shaved dorsal skin of rats. The following activities were assayed:

1. suppression of the carrageenan or hydroxylapatite paw oedemas;
2. reduction of chronic inflammation in established adjuvant arthritis;
3. local skin toxicity.

Cu(II) was an essential component. Some limited structure-activity correlations were made among alternative cupriphores. DMSO solutions of copper complexes were more potent than their solutions in ethanol. Glycerol was a beneficial additive. Reducing the acidity of some copper salicylate formulations also reduced their potency. Niflumic acid and phenylbutazone were effective non-salicylate transcutaneous cupriphores.     

Cytoprotective and Antioxidant Effects of the Methanol Extract of Eremomastax Speciosa in Rats

Background

Ethno-botanical information shows that Eremomastax speciosa is used in the traditional management of various stomach complaints including gastro-duodenal ulcers.

Materials and Methods

In this study, we tested the cytoprotective potential of the whole plant methanol extract (100–200 mg/kg, p.o), against HCl/ethanol, absolute ethanol, cold/restraint stress rats, and pylorus legated rats pre-treated with indomethacin. The effects of the extract on gastric lesion inhibition, the volume of gastric juice, gastric pH, gastric acid output, mucus production and gastric peptic activity were recorded. Oxidative stress parameters were measured in blood and gastric tissue samples obtained from the animals in all the models tested.

Results

The extract significantly (p<0.05), reduced the formation of cold/restraint ulcers by (31–60%, inhibition), completely inhibited (100%) the formation of lesions induced by HCl/ethanol at the highest dose, but was less effective against absolute ethanol (22–46% inhibition). The extract (200 mg/kg), significantly reduced lesion formation (P<0.01), gastric acidity (P<0.01), and volume of gastric secretions (P<0.05), in the indomethacin/pylorus ligation model, and did not affect the activity of pepsin in gastric juice. Blood concentrations of antioxidant enzymes (catalase, SOD and GSH), increased significantly and MDA concentrations decreased in all models tested.

Conclusion

Cytoprotection by E. speciosa methanol extract was attributed to its ability to reduce acid secretion, and to enhance mucosal defence and in vivo antioxidant status.     

Renal function and Na−K-ATPase in rats after suprarenal ligation of inferior vena cava

To assess the effects of altered renal function on Na?K-ATPase, the following groups of rats were studied:

1. rats with suprarenal vena cava ligation (SVCL), la. DOCA-treated rats with SVCL,
2. rats with infrarenal vena cava ligation (IVCL),
3. rats with glycerol-induced acute renal failure,
4. rats with bilateral ureteric ligation, and
5. K-exalate-treated rats with SVCL.

In group 1, acute renal failure with hyperkalemia developed and medullary Na?K-ATPase increased from 95±5 in control to 155±7 μmol Pi/mg prot//h,P<0.001, DOCA did not prevent the increase of Na?K-ATPase. In group 2, medullary Na?K-ATPase decreased from 130±10 in control to 88±7,P<0.01, in rats with IVCL. In group 3, cortical Na?K-ATPase decreased from 55±5 to 27±6,P<0.02. In group 4, Na?K-ATPase was unchanged. In group 5, maintenance of normokalemia prevented the rise in Na?K-ATPase. These experiments demonstrated a K-dependent activation of medullary Na?K-ATPase after SVCL but not in other forms of renal failure. Because SVCL diminishes drastically GFR per nephron, the present findings imply that increased loads of Na and K per nephron are not a prerequisite for an increase in medullary Na?K-ATPase. Hyperkalemia in presence of increased renal venous pressure seems to be causually related to the rise in medullary Na?K-ATPase activity.     

Dietary Selenium Deficiency Exacerbates Lipopolysaccharide-Induced Inflammatory Response in Mouse Mastitis Models

Selenium (Se) is an essential micronutrient that plays a critical role in anti-inflammatory processes and antioxidant defense system. In this study, we investigated the effects of dietary selenium deficiency on lipopolysaccharide (LPS)-induced mastitis in mouse models. Se content in the liver was assessed by fluorescent atomic absorption spectrometry. Glutathione peroxidase (GPx) activity in the blood, myeloperoxidase (MPO) activity, tumor necrosis actor alpha (TNF-α), and interleukin (IL)-1β in the supernatant of the mammary tissue were determined according to the corresponding kits. Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions were evaluated by Western blotting. The results showed that the Se-deficient mouse model was successfully replicated, and selenium deficiency exacerbated mammary gland histopathology, increased the expressions of TNF-α and IL-1β, and facilitated the activation of iNOS and COX-2 in LPS-induced mouse mastitis. In conclusion, our studies demonstrated that selenium deficiency resulted in more severe inflammatory response in LPS-induced mouse mastitis.     

Chronic intermittent ethanol exposure alters CA1 synaptic transmission in rat hippocampal slices

We investigated the neuroadaptive changes in synaptic transmission in the CA1 region of the hippocampus as a result of chronic intermittent ethanol exposure. Male Wistar rats were exposed daily (14 h) to ethanol vapors (blood alcohol levels = 150-200 mg%) for 12-14 days, and synaptic field potentials elicited by Schaffer collateral stimulation were compared in hippocampal slices from control and chronic ethanol-treated rats. Excitatory postsynaptic responses of slices were recorded under three conditions: (i) normal physiological saline; (ii) continued presence of 33 mM (150 mg%) ethanol (chronic ethanol-treated rats only); (iii) acute exposure to 33 mM ethanol. When recorded in ethanol-free physiological saline, the mean amplitude of the dendritic synaptic potential and the somatic population spike were significantly smaller in slices from chronic ethanol-treated rats compared to slices from control rats. Under conditions of continuous ethanol exposure, somatic and dendritic synaptic responses of slices taken from chronic ethanol-treated rats were further depressed, suggesting that neural pathways in area CA1 remained sensitive to ethanol. Acute application of ethanol led to a more pronounced reduction of the mean somatic population spike amplitude in slices from chronic ethanol-treated rats than in slices from control rats. However, dendritic synaptic responses were unaffected by acute ethanol in slices from both control and chronic ethanol-treated rats. In addition, we examined the involvement of presynaptic mechanisms in the effects of chronic intermittent ethanol using paired-pulse protocols. When recorded in the continued presence of ethanol, slices from chronic ethanol-treated rats exhibited a significant reduction in paired-pulse facilitation of the dendritic synaptic response compared to slices from control rats, indicating a presynaptic component to the neuroadaptive effects of chronic intermittent ethanol exposure. Conversely, acute ethanol exposure resulted in an enhancement of paired-pulse facilitation of the dendritic synaptic response, an effect that was similar in slices from both control and chronic ethanol-treated rats. Paired-pulse facilitation of the somatic population spike amplitude was not altered by chronic ethanol treatment. However, acute ethanol exposure significantly enhanced paired-pulse facilitation of the somatic population spike in slices from chronic ethanol-treated rats. This effect of acute ethanol was not observed in slices from control rats. Paired-pulse inhibition was not significantly altered in slices from chronic ethanol-treated rats, suggesting that GABAergic inhibitory mechanisms were not involved in the neuroadaptive effects of chronic intermittent ethanol exposure. We suggest that chronic intermittent ethanol exposure can induce multiple neuroadaptive changes in synaptic transmission of CA1 pyramidal neurons that are detectable at both the pre- and postsynaptic levels. Alterations in paired-pulse facilitation indicate presynaptic changes involving the release of the excitatory neurotransmitter glutamate, whereas changes in dendritic synaptic responses suggest postsynaptic changes in the responsiveness of neurons to synaptic input. Moreover, differential effects of chronic ethanol treatment on synaptic responses recorded in the dendrites versus the somatic region implicate additional effects of ethanol on somatically located mechanisms of CA1 pyramidal neurons. Furthermore, we suggest that complete tolerance to ethanol does not occur in the CA1 region of the hippocampus following chronic intermittent ethanol exposure.     

Antihyperlipidemic effects of mature coconut water and its role in regulating lipid metabolism in alloxan-induced experimental diabetes

The present study aims to evaluate the antihyperipidemic effects of mature coconut water (MCW), a natural nutritious beverage and its role in regulating lipid metabolism in experimental diabetes. The experimental animals were divided into four groups—normal control, MCW-alone-treated rats, diabetic control, and diabetic rats treated with MCW. Blood glucose, lipid profile, atherogenic index, phospholipids in various tissues, free fatty acids, activities of various lipogenic enzymes, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase in liver, lecithin–cholesterol acyl transferase (LACT) in plasma, and lipoprotein lipase (LPL) in heart were evaluated in all the experimental groups. The results indicate that in diabetic rats, MCW treatment reduced the blood glucose and lipid levels in blood and other tissues along with reduced activity of HMG CoA reductase and increased activity of LACT and LPL. In addition, levels of triglycerides, phospholipids, and free fatty acids in various tissues and atherogenic index were significantly lowered. In conclusion, MCW significantly reduced hyperlipidemia and regulated the defects in lipid metabolism in diabetic rats, indicating the therapeutic potential of MCW in diabetes and associated atherogenic complications.     

Characteristics of γδ T cells in Schistosoma japonicum-infected mouse mesenteric lymph nodes

Gamma delta (γδ) T cells are mainly present in mucosa-associated lymphoid tissues, which play an important role in mucosal immunity. In this study, C57BL/6 mice were infected by Schistosoma japonicum and lymphocytes were isolated from the mesenteric lymph node (MLN) to identify changes in the phenotype and function of γδ T cells using flow cytometry. Our results indicated that the absolute number of γδ T cells from the MLNs of infected mice was significantly higher compared with normal mice (P?P?+ γδ T cells (P?IFN-γ), interleukin (IL)-4, IL-9, and IL-17 in response to propylene glycol monomethyl acetate (PMA) plus ionomycin simulation, and the levels of IL-4, IL-9, and IL-17 increased significantly after S. japonicum infection (P?S. japonicum infection could induce γδ T cell activation, proliferation, and differentiation in the MLN. Moreover, our results indicated that the expression of NKG2D (CD314) was not increased in γδ T cells after infection, suggesting that other mechanisms are involved in activating γδ T cells. Furthermore, higher expression of programmed death-1 (CD279) but not IL-10 was detected in the γδ T cells isolated from infected mice (P?S. japonicum infection.