d-α-生育酚对乙醇引发的肝脏氧化应激的影响

目的观察d-α-生育酚对乙醇诱发的小鼠肝脏氧化应激的影响并探讨其机制。方法昆明种小鼠每天给予2.4g.kg-1bw乙醇后,再给予3个不同剂量的d-α-生育酚(25、50、100mg·kg-1bw.d-1),同时设正常对照组和乙醇对照组(乙醇2.4g·kg-1bw.d-1),连续灌胃60d后,测定肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、Na+,K+-ATP酶(Na+,K+-ATPase)、Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)、谷胱甘肽-S转移酶(GST)活力及丙二醛(MDA)的含量。结果小鼠摄入乙醇60d后,肝脏氧化应激水平明显增高。除Ca2+,Mg2+-ATPase以外,其余各项指标与正常对照组相比,差异均有显著性(P<0.05)。50mg·kg-1bw.d-1d-α-生育酚干预后,与乙醇对照组相比,GSH-Px、SOD、GST、Na+,K+-ATPase活力明显升高,MDA含量显著下降。其中,GSH-Px、Na+,K+-ATPase、MDA等3个指标在25mg·kg-1bw.d-1d-α-生育酚干预时亦出现同样的变化。结论适宜剂量的d-α-生育酚可以通过直接抑制脂质过氧化对乙醇诱发的肝脏氧化应激起保护作用。     

Anti-inflammatory effect of cinnamaldehyde and linalool from the leaf essential oil of Cinnamomum osmophloeum Kanehira in endotoxin-induced mice

Cinnamomum osmophloeum Kanehira is a Taiwan native plant that belongs to genus Cinnamomum and is also known as pseudocinnamomum or indigenous cinnamon. Its leaf is traditionally used by local people in cooking and as folk therapy. We previously demonstrated the chemical composition and anti-inflammatory effect of leaf essential oil of Cinnamomum osmophloeum Kanehira of linalool chemotype in streptozotocin-induced diabetic rats and on endotoxin-injected mice. The aim of the present study is to evaluate whether cinnamaldehyde and linalool the active anti-inflammatory compounds in leaf essential oil of Cinnamomum osmophloeum Kanehira. Before the injection of endotoxin, C57BL/6 mice of the experimental groups were administered cinnamaldehyde (0.45 or 0.9 mg/kg body weight) or linalool (2.6 or 5.2 mg/kg body weight), mice of the positive control group were administered the leaf essential oil (13 mg/kg body weight), and mice of the negative group were administered vehicle (corn oil, 4 mL/kg body weight) by gavage every other day for two weeks. All mice received endotoxin (i.p. 10 mg/mL/kg body weight) the next day after the final administration and were killed 12 h after the injection. Normal control mice were pretreated with vehicle followed by the injection with saline. None of the treatment found to affect body weight or food or water intake of mice before the injection of endotoxin. Cinnamaldehyde and linalool were found significantly reversed endotoxin-induced body weight loss and lymphoid organ enlargement compared with vehicle (P < 0.05). Both compounds also significantly lowered endotoxin-induced levels of peripheral nitrate/nitrite, interleukin (IL)-1β, IL-18, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and High-mobility group box 1 protein (HMGB-1), and levels of nitrate/nitrite, IL-1β, TNF-α, and IFN-γ in spleen and mesenteric lymph nodes (MLNs) (P < 0.05). Endotoxin-induced expression of toll-like receptor 4 (TLR4), Myeloid differentiation primary response gene 88 (MyD88), myeloid differentiation protein 2 (MD2), Nod-like receptor family, pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), and caspase-1 in spleen and mesenteric lymph nodes (MLNs) were inhibited by all tested doses of cinnamaldehyde and linalool (P < 0.05). Subsequently, the activation of nuclear factor (NF)-κB and the activity of caspase-1 in spleen and MLNs were also suppressed by these two compounds (P < 0.05). In addition, cinnamaldehyde and linalool at the dose equivalent to their corresponding content in the tested dose of the leaf essential oil, which was 0.9 mg/kg and 5.2 mg/kg, respectively, showed similar or slightly less inhibitory activity for most of these inflammatory parameters compared with that of the leaf essential oil. Our data confirmed the potential use of leaf essential oil of Cinnamomum osmophloeum Kanehira as an anti-inflammatory natural product and provide evidence for cinnamaldehyde and linalool as two potent agents for prophylactic use in health problems associated with inflammations that being attributed to over-activated TLR4 and/or NLRP3 signaling pathways.     

海狗油对实验性大鼠脂肪肝的抗脂质过氧化作用

目的:探讨海狗油对实验性大鼠脂肪肝的抗脂质过氧化作用及抗脂肪肝的作用机制。方法:小剂量四氯化碳合并高脂饲料建立大鼠脂肪肝模型,7周后,模型组ig等体积橄榄油、阳性药组ig辛伐他汀4mg·kg-1·d-1、海狗油低(L)、中(M)、高(H)剂量组分别ig海狗油0.5,1.6,4.8g·kg-1·d-1,连续8周,正常大鼠作为空白组。测定血清和肝脏中的丙二醛(MDA)、游离脂肪酸(FFA)、超氧化物歧化酶(SOD)、肝细胞色素P450 2E1(CYP2E1)免疫组化表达水平及脂肪肝指标即肝TC、TG、肝重、肝脏系数和组织学检查。结果:海狗油各治疗组与模型组相比血清和肝组织的MDA、FFA含量显著降低,SOD活性升高,CYP2E1免疫组化表达减弱。与之相应,大鼠脂肪肝指标肝重减轻,TC、TG减少,组织学检查显示肝细胞脂变程度显著减轻。结论:海狗油可诱导抗氧化酶SOD的活性,清除过多的氧自由基,从而减轻实验性脂肪肝症状,具有抗脂质过氧化作用。     

Alleviation of cell damage in experimental ANP in rats by administration of chondroitin-sulfate reduces

In order to explore the effects of retrograde infusion of chondroitin-sulfate via the pancreatic duct on cytoprotection and attenuation of oxidative damage during acute necrotic pancreatitis (ANP), male Wistar rats were randomly divided into three groups: A, B (experimental groups) and C (sham operation, control group). The rats in group A was subjected to retrograde injection of 5% sodium taurocholate via the pancreatic duct, and those in group B received chondroitin-sulfate therapy after ANP induction. All rats in three groups were killed at 6 h. The levels of malondialdehyde (MAD), total superoxide dismutase (SOD), glutathione (GSH), adenosine triphosphate (ATP) and serum amylase (SAM) were measured. The morphologic changes in pancreatic tissues were observed. It was found that the level of SAM was increased in group A and group B, with corresponding pathological changes of ANP. The levels of ATP, GSH and SOD in group A were decreased markedly and MDN increased significantly as compared with those in group B (P<0.01). In group B, the histopathologic damage was attenuated to a certain extent in comparison to that in group A. It was concluded that endogenous antioxidants were significantly reduced and lipid peroxidation increased during ANP. Retrograde infusion of chondroitin-sulfate via pancreatic duct could alleviate the pancreatic cell damage as a sort of scavengers of oxygen free radicals. Translated from J Chin Med Univ, 2006, 35(3): 297–298, 301 [译自: 中国医科大学学报]     

丹酚酸A对大鼠脑突触体和线粒体氧应激损伤的体外保护作用

利用蔗糖梯度法分离大鼠脑突触体和线粒体，以Fe^2＋-半胱氨酸（Cys）为氧自由基生成系统造成大鼠脑突触体和线粒体氧应激损伤模型. 在体外Fe^2＋-Cys与脑突触体和线粒体共同温孵可使丙二醛(MDA)生成量显著增加，线粒体ATP酶活性下降. 预先加入丹酚酸 A(Sal A)可显著抑制MDA生成，恢复线粒体 ATP酶活性，防止线粒体肿胀和膜流动性的降低. 通过电镜照片可看到Fe^2＋-Cys引起的线粒体和突触体结构病理性改变，预先加入Sal A可减轻Fe^2＋-Cys造成的这一损伤. 此外，Sal A可阻抑H₂O₂引起的脑突触体GSH含量的降低. 由此可见，Sal A体外对氧应激引起的大鼠脑突触体和线粒体脂质过氧化损伤有明显的保护作用.     

Glutathione metabolism in cyclosporine A-treated rats: dose- and time-related changes in liver and kidney

1. We investigated the simultaneous effects of cyclosporine A (CsA) treatment in rats on glutathione metabolism, oxidative status and their interorgan relationship in the liver and kidney. 2. Reduced and oxidized glutathione (GSH and GSSG, respectively), lipid peroxidation and the activity of several enzymes of the glutathione cycle were evaluated in adult Wistar rats treated daily (i.p.) with saline, CsA vehicle (olive oil) or CsA (10 and 20mg/kg per day) for either 1 or 4 weeks (short- and long-term treatments, respectively). 3. Cyclosporine A treatment elicited a significant depletion in liver GSH content and a decrease in the GSH/GSSG ratio that was unrelated to either the time of treatment or the dose used; these effects were already evident after 1 week of treatment. Renal GSH levels remained unaffected or increased, while those of GSSG increased markedly in all CsA-treated rats, leading to decreases in the GSH/GSSG ratio, except in rats treated in the short term with the lower dose of CsA. These changes in the GSH/GSSG ratio were time and dose dependent. Short-term CsA treatment using the higher dose and long-term treatment with both doses of CsA progressively enhanced lipid peroxidation, which was reflected by increased levels of thiobarbituric acid-reactive substances in both hepatic and renal homogenates. Hepatic gamma-glutamylcysteine synthetase activity was increased after long-term treatment with both doses of CsA, whereas the activity of GSH hepatic peroxidase and GSH transferase was not significantly modified in any of the experimental groups. In contrast, renal gamma-glutamyl transpeptidase activity decreased in a progressive fashion, with the magnitude of this decrease being dose and time dependent. The plasma levels of total glutathione increased only in rats treated in the long term, regardless of the dose of CsA used, and remained unaltered in animals treated in the short term. 4. In summary, the data collected indicate that CsA treatment alters the interorgan homeostasis of glutathione and the oxidative status of the rat liver and kidney, which is associated with increases in lipid peroxidation in both organs, and also induces modifications in the activity of some enzyme related to the glutathione cycle.     

Comparison of acute oxidative stress on rat lung induced by nano and fine-scale,soluble and insoluble metal oxide particles: NiO and TiO2

The aim of the present study is to understand the association between metal ion release from nickel oxide (NiO) nanoparticles and induction of oxidative stress in the lung. NiO nanoparticles have cytotoxic activity through nickel ion release and subsequent oxidative stress. However, the interaction of oxidative stress and nickel ion release in vivo is still unclear. In the present study, we examined the effect of metal ion release on oxidative stress induced by NiO nanoparticles. Additionally, nano and fine TiO₂ particles as insoluble particles were also examined. Rat lung was exposed to NiO and TiO₂ nanoparticles by intratracheal instillation. The NiO nanoparticles released Ni²⁺ in dispersion. Bronchoalveolar lavage fluid (BALF) was collected at 1, 24, 72 h and 1 week after instillation. The lactate dehydrogenase (LDH) and HO-1 levels were elevated at 24 and 72 h after instillation in the animals exposed to the NiO nanoparticles. On the other hand, total hydroxyoctadecadienoic acid (tHODE), which is an oxidative product of linoleic acid, as well as SP-D and α-tochopherol levels were increased at 72 h and 1 week after instillation. Fine NiO particles, and nano and fine TiO₂ particles did not show lung injury or oxidative stress from 1 h to 1 week after instillation. These results suggest that Ni²⁺ release is involved in the induction of oxidative stress by NiO nanoparticles in the lung. Ni²⁺ release from NiO nanoparticles is an important factor inoxidative stress-related toxicity, not only in vitro but also in vivo.     

Long-term exposure to repetitive hyperbaric oxygen results in cumulative oxidative stress in rat lung tissue

Context: Despite its known benefits, hyperbaric oxygen (HBO) is also reported to enhance the production of reactive oxygen species and can cause oxidative stress in several tissues. Previous studies had shown that HBO-induced oxidative stress is directly proportional to both its exposure pressure and duration. Nevertheless, these studies were usually performed with single-session HBO exposure but its clinical use commonly depends on long-term exposure periods.

Objective: To clarify the oxidative effect of long-term repetitive HBO in the lung tissue of rats.

Materials and methods: Male Sprague-Dawley rats were divided into six study groups exposed to consecutive HBO sessions (2.8 atm/90?min) for 5, 10, 15, 20, 30, and 40 days. Animals were sacrificed 24?h after the last HBO session. An additional control group was set to obtain normal data. Lung malondialdehyde (MDA) and carbonylated protein (PCC) levels were determined as measures of oxidative stress along with the activities of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase.

Results: None of the measured parameters showed any changes among the groups exposed to 5–15 HBO sessions. However, MDA, PCC, and SOD were found to be significantly increased in the 20 to 40 session groups.

Discussion and conclusion: These results indicate that repetitive treatment with HBO may cause oxidative stress in critical tissues including the lung. Although HBO-mediated free radicals are accepted to be responsible for the benefits of this therapeutic modality, especially in cases with prolonged exposure, possible injurious effects of supranormal values of bio-oxidative products need to be considered.     

Antioxidant and hepatoprotective effects of Solanum xanthocarpum leaf extracts against CCl4-induced liver injury in rats

Context: Solanum xanthocarpum Schard. and Wendl. (Solanaceae) has been used in traditional Indian medicines for its antioxidant, anti-inflammatory, and antiasthmatic properties.

Objective: The present study demonstrates the antioxidant and hepatoprotective effects of S. xanthocarpum. On the basis of in vitro antioxidant properties, the active fraction from column chromatography of the methanol extract of S. xanthocarpum leaves (SXAF) was chosen as the potent fraction and used for hepatoprotective studies in rats.

Materials and methods: The antioxidant activity was evaluated by 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 2,2-diphenyl-1-picrylhydrazyl (DPPH), and reducing power assays. Rats were pre-treated with 100 and 200?mg/kg b.w. of SXAF for 14?d with a single dose of CCl₄ in the last day. Hepatoprotective properties were determined by serum biochemical enzymes, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), antioxidant enzymes (SOD, CAT, GSH, and GST), and histopathology studies.

Results: SXAF exhibited significant antioxidant activity in scavenging free radicals with IC₅₀ values of 11.72?µg (DPPH) and 17.99?µg (ABTS). Rats pre-treated with SXAF demonstrated significantly reduced levels of serum LDH (1.7-fold), ALP (1.6-fold), and AST (1.8-fold). Similarly, multiple dose SXAF administration at 200?mg/kg b.w. demonstrated significantly enhanced levels of SOD (1.78?±?0.13), CAT (34.63?±?1.98), GST (231.64?±?14.28), and GSH (8.23?±?0.48) in liver homogenates. Histopathological examination showed lowered liver damage in SXAF-treated groups.

Discussion and conclusion: These results demonstrate that SXAF possesses potent antioxidant properties as well as hepatoprotective effects against CCl₄-induced hepatotoxicity.     

Lophirones B and C prevent aflatoxin B1-induced oxidative stress and DNA fragmentation in rat hepatocytes

Context Despite the reported anticarcinogenic activity of lophirones B and C, no scientific information exists for its activity in rat hepatocytes.

Objective Effect of lophirones B and C on aflatoxin B₁ (AFB₁)-induced oxidative stress, and DNA fragmentation in rat hepatocytes was investigated.

Materials and methods Wistar rat hepatocytes were incubated with lophirones B and C (1?mg/mL) or sylimarin (1?mg/mL) in the presence or absence of AFB₁. For an in vivo study, rats were orally administered with lophirones B and C, and/or AFB₁ (20?μg/d) for 9 weeks.

Results Lophirones B and C lowered AFB₁-mediated increase in nitric oxide, superoxide anion radicals, caspase-3 and fragmented DNA. Lophirones B and C attenuated AFB₁-mediated decrease in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and reduced glutathione. Also, lophirones B and C attenuated AFB₁-mediated increase in conjugated dienes, lipid hydroperoxides and malondialdehyde in rat hepatocytes. Furthermore, AFB₁-mediated alterations in alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, albumin, total bilirubin and globulin in rat serum were significantly annulled in lophirones B and C-treated rats.

Conclusion This study revealed that lophirones B and C prevented AFB₁-induced oxidative damage in rat hepatocytes.     

Chemical composition and biological activities of Asimina triloba leaf essential oil

Leaf essential oil of Asimina triloba (L.) Dunal (F. Annonaceae) was found to be active against both human lung carcinoma and breast carcinoma cell lines. From this hydrodistillation extract, 37 components were identified by GC-MS analysis; sesquiterpenes dominated the oil composition (83%), with cadinene derivatives occurring in the greatest abundance (70%). Using the DDPH assay for antioxidant testing, the essential oil displayed moderate activity relative to vitamin E. These findings suggest that A. triloba essential oil may provide leads for active anticancer agents.     

Alteration of lipid status and lipid metabolism,induction of oxidative stress and lipid peroxidation by 2,4-dichlorophenoxyacetic herbicide in rat liver

Abstract

This study aims to investigate the effects of the 2,4-dichlorophenoxyacetic herbicide (2,4-D) on plasma lipids, lipoproteins concentrations, hepatic lipid peroxidation, fatty acid composition and antioxidant enzyme activities in rats. Animals were randomly divided into four groups of 10 each: control group and three 2,4-D-treated groups G1, G2 and G3 were administered 15, 75 and 150?mg/kg/BW/d 2,4-D by gavage for 28?d, respectively. Results showed that 2,4-D caused significant negative changes in the biochemical parameters investigated. The malondialdehyde level was significantly increased in 2,4-D-treated groups. Fatty acid composition of the liver was also significantly changed with 2,4-D exposure. Furthermore, the hepatic antioxidant enzyme activities were significantly affected. Finally, 2,4-D at the studied doses modifies lipidic status, disrupt lipid metabolism and induce hepatic oxidative stress. In conclusion, at higher doses, 2,4-D may play an important role in the development of vascular disease via metabolic disorder of lipoproteins, lipid peroxidation and oxidative stress.     

Curcumin, the active principle of turmeric (Curcuma longa), ameliorates diabetic nephropathy in rats

Chronic hyperglycaemia in diabetes leads to the overproduction of free radicals and evidence is increasing that these contribute to the development of diabetic nephropathy. Among the spices, turmeric (Curcuma longa) is used as a flavouring and colouring agent in the indian diet every day and is known to possess anti-oxidant properties. The present study was designed to examine the effect of curcumin, a yellow pigment of turmeric, on renal function and oxidative stress in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced by a single intraperitoneal injection of STZ (65 mg/kg) in rats. Four weeks after STZ injection, rats were divided into four groups, namely control rats, diabetic rats and diabetic rats treated with curcumin (15 and 30 mg/kg, p.o.) for 2 weeks. Renal function was assessed by creatinine, blood urea nitrogen, creatinine and urea clearance and urine albumin excretion. Oxidative stress was measured by renal malonaldehyde, reduced glutathione and the anti-oxidant enzymes superoxide dismutase and catalase. Streptozotocin-injected rats showed significant increases in blood glucose, polyuria and a decrease in bodyweight compared with age-matched control rats. After 6 weeks, diabetic rats also exhibited renal dysfunction, as evidenced by reduced creatinine and urea clearance and proteinuria, along with a marked increase in oxidative stress, as determined by lipid peroxidation and activities of key anti-oxidant enzymes. Chronic treatment with curcumin significantly attenuated both renal dysfunction and oxidative stress in diabetic rats. These results provide confirmatory evidence of oxidative stress in diabetic nephropathy and point towards the possible anti-oxidative mechanism being responsible for the nephroprotective action of curcumin.     

Quercetin protects human peripheral blood mononuclear cells from OTA‐induced oxidative stress,genotoxicity, and inflammation

Ochratoxin A (OTA) is one of the most abundant food‐contaminating mycotoxins world wide, and is detrimental to human and animal health. This study evaluated the protective effect of quercetin against OTA‐induced cytotoxicity, genotoxicity, and inflammatory response in lymphocytes. Cytotoxicity determined by MTT assay revealed IC₂₀ value of OTA to be 20 µM, which was restored to near control values by pretreatment with quercetin. Oxidative stress parameters such as antioxidant enzymes, LPO and PCC levels indicated that quercetin exerted a protective effect on OTA‐induced oxidative stress. Quercetin exerted an antigenotoxic effect on OTA‐induced genotoxicity, by significantly reducing the number of structural aberrations in chromosomes and comet parameters like, % olive tail moment from 2.76 ± 0.02 to 0.56 ± 0.02 and % tail DNA from 56.23 ± 2.56 to 12.36 ± 0.56 as determined by comet assay. OTA‐induced NO, TNF‐α, IL‐6, and IL‐8 were significantly reduced in the quercetin pretreated samples indicating its anti‐inflammatory role. Our results demonstrate for the first time that quercetin exerts a cytoprotective effect against OTA‐induced oxidative stress, genotoxicity, and inflammation in lymphocytes. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 855–865, 2016.     

Brassica nigra plays a remedy role in hepatic and renal damage

Context: Black mustard [Brassica nigra (L.) Koch] of the Brassicaceae (Cruciferae) family is commonly used as a spice and a cheap source of antimicrobial agents for bacterial infections.

Objectives: The present investigation was to demonstrate the protective effect of the methanol extract of B. nigra leaves against d-galactosamine (d-GalN)-induced hepatic and nephrotoxicity in Wistar rats.

Methods: Activity of the methanol extract of B. nigra at doses of 200 and 400 mg/kg b.wt. against d-GalN (500 mg/kg b.wt.) induced toxicity, with silymarin used as the standard. Histological damage, activities of serum marker enzyme, hematological changes, metabolites such as bilirubin, urea, uric acid, and creatinine levels, tissue thiobarbutric acid reactive substance, enzymic and non-enzymic antioxidants and inflammatory marker enzymes such as myeloperoxidase, cathepsin D, and acid phosphatase were assessed.

Results: The d-GalN-induced toxicity was evident from a significant increase (p < 0.001) in the serum and tissue inflammatory markers in toxic rats, when compared with the control (saline alone treated animals). The B. nigra pretreated groups (200 and 400 mg/kg b.wt.) showed significant (p < 0.001) reduction in the d-GalN-induced toxicity as obvious from biochemical parameters. Histopathological observations confirm the protective effect of B. nigra leaf extract by reduction in hepatic and renal tissue damage. Experimentals extract showed a similar effect as the standard.

Conclusions: The crude methanol extract of B. nigra leaf lacks inherent toxicity and exhibits hepatic and nephroprotective effects against d-GalN-induced toxicity in Wistar rats.     

Smokeless tobacco impairs the antioxidant defense in liver, lung, and kidney of rats.

The present study was designed to evaluate the effects of long-term use of aqueous extract of gutkha (a form of smokeless tobacco) on the antioxidant defense status and histopathological changes in liver, lung, and kidney of male Wistar rats. Animals were orally administered aqueous extract of smokeless tobacco (AEST) at a low dose (96 mg/kg body weight per day) for 2 and 32 weeks, and at a high dose (960 mg/kg body weight per day) for 2 weeks. High-dose AEST for 2 weeks decreased the hepatic glutathione (GSH) and glutathione peroxidase (GPx), and increased lipid peroxidation (Lpx) by 17%, 19%, and 20%, respectively. Low-dose AEST for 32 weeks significantly decreased (p < 0.05) the antioxidant status in these organs. In liver, AEST decreased GSH levels and the activities of superoxide dismutase (SOD), catalase (CAT), and GPx by 34.6%, 29%, 17.1%, and 17.4%, respectively, but it increased Lpx by 64%. In kidney, GSH, SOD, CAT, and GPx were decreased by 26.6%, 23%, 33%, and 18%, respectively, with an increase of Lpx by 65%. AEST decreased the lung GSH, SOD, CAT, and GPx, and increased lung Lpx by 43%, 28.5%, 37%, 40%, and 24%, respectively. However, no change in the plasma levels of vitamins A, C, and E were observed with AEST treatment. Histopathological findings suggest that administration of AEST at the high dose for 2 weeks or at the low dose for 32 weeks could cause mild to moderate inflammation in liver and lungs. In conclusion, a decrease in the antioxidant defense system and long-term inflammation caused by smokeless tobacco may be risk factors for gutkha-induced pathogenesis.     

Exploration of antimicrobial potential of essential oils of Cinnamomum glanduliferum,Feronia elephantum,Bupleurum hamiltonii and Cyclospermum leptophyllum against foodborne pathogens

Abstract

Context: Cinnamomum glanduliferum (Wall.) Meissn. (Lauraceae), Feronia elephantum Correa (Rutaceae), Bupleurum hamiltonii Balak (Apiaceae) and Cyclospermum leptophyllum (Pers.) Sprague ex Britton & P. Wilson (Apiaceae) are common species found in Northwest Himalaya and are widely used as folk medicine. The study became more interesting because hitherto there are no reports on the antimicrobial screening of these species with specific chemical composition.

Objective: The antimicrobial potential of the essential oils of C. glanduliferum, F. elephantum, B. hamiltonii and C. leptophyllum against some commonly occurring foodborne pathogenic and spoilage bacteria was explored in this study.

Materials and methods: Antimicrobial screening studies of essential oils were performed against some Gram-positive and Gram-negative bacterial strains using broth-dilution methods. Each essential oil was prepared by serial double dilution method to get final concentrations ranging from 0.85--440.0?µg/ml in a 96 microtiter plate.

Results: The in vitro studies revealed that C. glanduliferum oil was very active against Gram-negative bacteria, A. salmonicida (MIC 1.72?µg/ml), E. coli (MIC 3.43?µg/ml), and P. aeruginosa (MIC 3.43?µg/ml) as compared to the standards gentamicin and kanamicin. Oil of C. leptophyllum exhibited better inhibitory activity profile against Gram-positive S. aureus (MIC 3.43?μg/ml) and Gram-negative E. herbicola (MIC 1.72?μg/ml) and P. aeruginosa (MIC 3.43?μg/ml) as compared to the standards.

Discussion and conclusion: These results reveal that these essential oils may be used in the treatment of diseases caused by the foodborne pathogenic and spoilage bacteria. Their importance as potential medicinal agents is based on the antimicrobial findings.     

生理浓度的糖皮质激素对大鼠肺泡上皮细胞炎症因子生成的抑制作用

目的探讨生理浓度下糖皮质激素对脂多糖(lipopo-lysaccharide,LPS)诱导大鼠肺泡上皮细胞IL-6表达的影响及其机制。方法LPS、生理浓度的氢化可的松、过氧化氢等处理细胞,ELISA测定细胞上清IL-6水平,并对细胞组蛋白去乙酰化酶(histone deacetylase,HDAC)的活性进行测定。结果与对照组相比LPS明显诱导细胞IL-6的蛋白表达(P<0·01)。生理浓度氢化可的松明显降低LPS诱导的IL-6蛋白水平表达的作用(P<0·01)。HDAC抑制剂(Trichosta-tin,TSA)明显拮抗氢化可的松的这种作用(P<0·01);与对照相比,LPS明显下调HDAC的活性(P<0·01),糖皮质激素抑制LPS下调HDAC活性的作用(P<0·01);过氧化氢增强LPS诱导IL-6蛋白表达的作用(P<0·01),过氧化氢、LPS和氢化可的松共同处理细胞后,其IL-6的浓度较LPS与H2O2共同刺激组差别无统计学意义(P>0·05)。过氧化氢浓度依赖性地降低细胞HDAC活性(P<0·01)。结论生理浓度的糖皮质激素同样具有抗炎作用,氧化应激可抑制糖皮质激素抗炎作用,具体机制可能与其降低HDAC活性有关,这些机制可能在与氧化应激有关的呼吸系统疾病中发挥重要作用。     

Selenium and rutin alone or in combination do not have stronger protective effects than their separate effects against cadmium-induced renal damage

Context: Selenium (Se) and rutin (RUT) are antioxidants that protect against tissue damage.

Objective: In this study, the separate and combine protective effects of RUT and Se against cadmium (Cd)-induced renal damage were evaluated in rats.

Materials and methods: Wistar rats were treated by gavage to RUT (30?mg/kg) or Se (0.15?ppm) or Cd (200?ppm) in drinking water alone or in combination (30?mg/kg RUT?+0.15?ppm Se?+?200?ppm Cd). Corn oil was used as vehicle (2?mL/kg). After a 5-week treatment period, rat kidneys were removed for biochemical assays and histopathological examination. Se and Cd levels were evaluated by flame atomic absorption spectrophotometry.

Results: The malondialdehyde and glutathione levels as well as superoxide dismutase and catalase activities in the Cd-treated animals were increased compared with control values (0.056?±?0.0003 versus 0.011?±?0.0005?μmol/mg; 0.005?±?0.0006 versus 0.00085?±?0.0002?μg/mg; 1.62?±?0.09 versus 0.48?±?0.12 units/mg; 650?±?25 versus 361.89?±?31?μmol H₂O₂/mg, respectively). Cd treatment was also associated with decreased renal Se concentration (4.19?±?0.92 versus 7.73?±?0.7?μg/g dry weight), increased alkaline phosphatase (0.07?±?0.0015 versus 0.033?±?0.0019 unit/mg), acid phosphatase (0.029?±?0.0021 versus 0.015?±?0.0016 unit/mg), and lactate dehydrogenase (0.032?±?0.004 versus 0.014?±?0.0027 unit/mg) activities, respectively, and with evidence of severe renal damage. The combination of RUT and Se or their separate effects prevented the Cd-induced oxidative renal damage. However, their combine effects do not have stronger effects than their separate effect against Cd-induced renal damage.

Discussion and conclusion: RUT and Se function as potent antioxidant in the protection of renal damage induced by Cd.