Protective effect of Periplaneta americana extract in ulcerative colitis rats induced by dinitrochlorobenzene and acetic acid

Context: Periplaneta americana L. (Dictyoptera; Blattaria) has been traditional used to treat ulcers, burns and heart disease in southwestern China. Recent reports indicate that P. americana can be used as an alternative medicine in therapy of ulcerative colitis, but the mechanism involved remains obscure.

Objective: This study investigated the therapeutic effect of P. americana extract (PAE) in rat colitis and elucidated its potential mechanism.

Materials and methods: Dinitrochlorobenzene and acetic acid-induced colitis rat model was applied. Colitis rats were treated with PAE for 10 d and estimated disease activity index daily. Rectal inflammation was assessed by myeloperoxidase activity and histological changes. Another colitis rats were treated with PAE for 4 d, meanwhile gavage with Escherichia coli labelled with green fluorescent protein. Mesenteric lymph nodes, colon, liver, spleen and kidney were harvested for bacteria culture. PAE was suspended in distilled water then partitioned with ethyl acetate and n-butanol to obtain ethyl acetate fraction, n-butanol fraction and water fraction, respectively. Fibroblasts proliferation and collagen accumulation of each fraction was determined.

Results: PAE treatment reduced the severity of colitis and tissue myeloperoxidase accumulation (p?<?0.001). Also, PAE at 80?mg/kg significantly inhibited labelled E. coli from translocating to distant organs, especially to MLN and liver. Additionally, PAE significantly stimulated fibroblasts proliferation (126.9%) and collagen accumulation (130.8%) for 48?h incubation. Among the partitions, ethyl acetate fraction generally had higher fibroblast viability enhanced-activity.

Conclusions: PAE can protect against ulcerative colitis and this protection is attributed to anti-inflammation and fibroblasts viability.     

Protective effect of embelin against acetic acid induced ulcerative colitis in rats

The aim of the present study is to evaluate the effect of embelin isolated from Embelia ribes on acetic acid induced colitis in rats. Experimental animals received embelin (25 and 50 mg/kg, p.o.) and sulfasalazine (100 mg/kg, p.o.) for five consecutive days before induction of colitis by intra-rectal acetic acid (3% v/v) administration and the treatment continued up to 7 days. The colonic mucosal injury was assessed by clinical, macroscopic, biochemical and histopathological examinations. Embelin treatment significantly decreased clinical activity score, gross lesion score, percent affected area and wet colon weight when compared to acetic acid induced controls. The treatment also reduced significantly the colonic myeloperoxidase activity, lipid peroxides and serum lactate dehydrogenase and significantly increased the reduced glutathione. The histopathological studies also confirmed the foregoing findings. The protective effect may be due to its antioxidant and anti-inflammatory activities.     

Gallic acid attenuates chromium-induced thyroid dysfunction by modulating antioxidant status and inflammatory cytokines

Hexavalent chromium-mediated oxidative stress causes severe organ damage. The present study was designed to investigate the possible thyroprotective effect and underlying mechanisms of gallic acid using rat model of potassium dichromate-induced thyroid dysfunction. Forty adult male albino rats were divided into 4 groups: control, gallic acid (20 mg GA/kg b. wt), potassium dichromate (2 mg PD/kg b. wt) and the fourth group was co-treated with PD and GA. PD-injection resulted in decreased serum free triiodothyonine (FT3), free thyroxine (FT4) with concomitant significant increase in thyroid stimulating hormone (TSH) levels. Superoxide dismutase (SOD), glutathione-S-transferase (GST) activities and their respective mRNA expression and reduced glutathione (GSH) content were significantly decreased. Thyroid nitrosative stress marker (NO level and iNOS mRNA and protein expression) and pro-inflammatory cytokines (serum TNF-α, IL-6 and thyroid TNF-α, IL-6 and COX-2 gene and protein expression levels) were disturbed. Histopathological changes revealed distended, collapsed and degenerated follicles with vacuolated cytoplasm. GA co-treatment attenuated pro-inflammatory cytokines, the thyroid expression of iNOS, TNF-α, IL-6 and COX-2, decreased the elevated lipid peroxidation biomarkers and NO level and up- regulated SOD and GST mRNA expression levels. In conclusion, GA has shown strong modulatory potential against PD-induced inflammation and oxidative stress in albino rats.     

Effect of N-acetylcysteine on colitis induced by acetic acid in rats.

(1) To verify the proposed role of reactive oxygen species (ROS) in ulcerative colitis, the effect of an antioxidant N-acetylcysteine (NAC) was studied in acetic acid (AA)-induced colonic inflammation. (2) Depending on the dose used, NAC administered intracolonically was found to reduce the extent of colonic damage, along with a decrease in myeloperoxidase (MPO) activity, colonic wet weight and wet/dry weight ratio. (3) NAC attenuated the enhanced vascular permeability and prevented the depletion of colonic reduced glutathione (GSH) caused by AA administration. (4) The findings indicate that NAC may prove beneficial in the treatment of colitis.     

复方盐藻素对肺癌化疗中SOD和MDA活力的影响

近些年在世界范围内,非小细胞肺癌发病率呈逐年上升趋势,是严重威胁人类健康的疾病之一.当前,治疗方案是以手术为主的综合治疗,对于Ⅱ期、Ⅲa期患者术后常规行辅助化疗,一线治疗方案是铂类 第3代化疗药物如紫杉醇、长春瑞滨和吉西他滨等药物,均为细胞毒性药物,对正常骨髓细胞具有杀伤作用,容易导致化疗后出现骨髓抑制,严重者会并发感染、出血等并发症,给患者造成痛苦,影响进一步实施化疗,甚至少数病例会危及生命,目前尚无有效的预防策略.文献报道,盐藻素和维生素E可增强机体的免疫力,提高机体抗氧化能力,减缓化疗副作用的能力[1-3].因此本研究通过建立小鼠肺肿瘤模型及人体实验对含盐藻素和维生素E成分的药物:复方盐藻素对减轻肺癌化疗副作用的抗氧化机制进行了研究.     

Effect of ethanolic extract of leaves of Paederia foetida Linn. on acetic acid induced colitis in albino rats

Objectives:

To evaluate the effect of ethanolic extract of leaves of Paederia foetida on acetic acid induced colitis in albino rats.

Materials and Methods:

Ethanolic extract of Paederia foetida (EEPF) was prepared by percolation method. Acute toxicity test was done by using Organization for Economic Cooperation and Development guidelines. Albino rats were divided into four groups of five animals each. Groups A and B received 3% gum acacia. Groups C and D received EEPF 500 mg/kg body weight (BW) and 5-aminosalisylic acid 100 mg/kg BW respectively. Colitis was induced by transrectal administration of 4% acetic acid on 5^th day. All animals were sacrificed after 48 h of colitis induction and distal 10 cm of the colon was dissected. Colon was weighed for disease activity index (DAI) and scored macroscopically and microscopically. Biochemical assessment of tissue myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) was done in colonic tissue homogenate and malondialdehyde (MDA) was estimated in serum.

Results:

P. foetida showed significant (P < 0.05) reduction in DAI, macroscopic and microscopic lesion score as well as significant (P < 0.05) improvement in MPO, MDA, CAT, and SOD level as compared to Group B.

Conclusions:

The ethanolic extract of leaves of P. foetida showed significant amelioration of experimentally induced colitis, which may be attributed to its anti-inflammatory and antioxidant property.KEY WORDS: Antioxidant, colitis, Paederia foetida     

The new experimental ulcerative colitis model in rats induced by subserosal injection of acetic acid

Prostacyclin is an endogeneous eicosanoid synthesized by vascular endothelial cells, and has potent inhibitory effects on platelet adhesion/aggregation and vasoconstriction. However, its therapeutic use is restricted by its extremely short half-life. Beraprost sodium (beraprost) is the first orally active prostacyclin analogue developed by TORAY Industries, Inc. Beraprost possesses a phenol moiety instead of the exo-enol ether moiety, which is the cause of the instability of prostacyclin, and has a modified omega-side chain that contributes to dissociating antiplatelet action from adverse reactions. In 1992, beraprost was approved as a drug for chronic arterial occlusion. Beraprost is now widely used clinically as "Dorner" or "Procylin". The indication for "primary pulmonary hypertension" was also approved in 1999. Recently in Europe, a placebo controlled trial named "Beraprost et Claudication Intermittent-2 (BERCI-2)" was performed, and it was reported that beraprost improved the walking distances of the patients. Beraprost has a variety of biological activities such as antiplatelet effects, vasodilation effects, antiproliferative effects on vascular smooth muscle cells, cytoprotective effects on endothelial cells and inhibitory effects on the production of inflammatory cytokines. On the basis of basic and clinical research, it has been suggested that beraprost is also effective for many intractable diseases. We expect that the relationship between reduced prostacyclin level and these diseases would be clarified and the beneficial effects of beraprost would be demonstrated by controlled clinical trials in the future.     

The effects of selective cyclooxygenase-2 inhibitors, celecoxib and rofecoxib, on experimental colitis induced by acetic acid in rats

Several mediators may be involved in the pathogenesis of inflammatory bowel disease, as well as in experimental colitis. The present work was conducted to investigate the effects of the two selective cyclooxygenase-2 inhibitors, celecoxib and rofecoxib, on experimentally induced colitis in rats. Rectal instillation of acetic acid was used to induce the colitis. Acetic acid treatment caused haemorrhagic diarrhoea and weight loss in rats. Celecoxib (5 mg/kg) or rofecoxib (2.5 mg/kg), when given twice daily by the oral route, reduced the degree of haemorrhagic diarrhoea and the weight loss produced. In addition, they produced a significant reduction in the degree of colonic injury, the rise in myeloperoxidase (MPO) levels, total nitric oxide synthetase (NOS) activity, platelet-activating factor (PAF), histamine levels and prostaglandin E2 levels. In contrast, there was a significant increase in the levels of reduced glutathione (GSH). Thus, the findings of the present study provide evidence that selective cyclooxygenase-2 inhibitors may be beneficial in patients with inflammatory bowel disease.     

Phytochemical,antioxidant and protective effect of cactus cladodes extract against lithium-induced liver injury in rats

Context: Opuntia ficus-indica (L.) Mill. (Castaceae) (cactus) is used in Tunisian medicine for the treatment of various diseases.

Objective: This study determines phytochemical composition of cactus cladode extract (CCE). It also investigates antioxidant activity and hepatoprotective potential of CCE against lithium carbonate (Li₂CO₃)-induced liver injury in rats.

Materials and methods: Twenty-four Wistar male rats were divided into four groups of six each: a control group given distilled water (0.5?mL/100?g b.w.; i.p.), a group injected with Li₂CO₃ (25?mg/kg b.w.; i.p.; corresponding to 30% of the LD₅₀) twice daily for 30 days, a group receiving only CCE at 100?mg/kg of b.w. for 60 days and then injected with distilled water during the last 30 days of CCE treatment, and a group receiving CCE and then injected with Li₂CO₃ during the last 30 days of CCE treatment. The bioactive components containing the CCE were identified using chemical assays.

Results: Treatment with Li₂CO₃ caused a significant change of some haematological parameters including red blood cells (RBC), white blood cells (WBC), haemoglobin content (Hb), haematocrit (Ht) and mean corpuscular volume (VCM) compared to the control group. Moreover, significant increases in the levels of glucose, cholesterol, triglycerides and of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) activities were observed in the blood of Li₂CO₃-treated rats. Furthermore, exposure to Li₂CO₃ significantly increased the LPO level and decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in the hepatic tissues.

Conclusion: CCE possesses a significant hepatoprotective effect.     

The protective action of scutellarin against immunological liver injury induced by concanavalin A and its effect on pro-inflammatory cytokines in mice

Scutellarin is a natural compound from a Chinese herb. The purpose of this paper was to study the protective effect of scutellarin on concanavalin A (Con A)-induced immunological liver injury and its effect on liver nuclear factor kappaB (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), and inducible nitric oxide synthase (iNOS) expression in mice. Mouse liver injury was produced by injection of Con A 25 mg kg-1 via the tail vein. Scutellarin 50 or 100 mg kg-1 was peritoneally administered to mice 9 or 1 h before injection of Con A. The levels of serum alanine aminotransferase (ALT) and asparatate aminotransferase (AST), NO2-/NO3- and TNF-alpha were determined with biochemical kits, and ELISA using Quantikine Mouse TNF-alpha kit according the manufacturer's instructions. Liver lesions were examined by light microscope. The expression of TNF-alpha, IFN-gamma, iNOS and Fas mRNA in the livers was detected by RT-PCR; and the expression of c-Fos, c-Jun, iNOS and IkappaB proteins was measured by Western Blotting. As a result, pretreatment with scutellarin 100 mg kg-1 significantly decreased the serum ALT, AST, NO2-/NO3- and TNF-alpha levels, and also reduced liver lesions induced by Con A. Scutellarin 100 mg kg-1 down-regulated expression of TNF-alpha and iNOS mRNA, and c-Fos, c-Jun and iNOS protein, while scutellarin enhanced the degradation of IkappaB in the livers of mice injected with Con A. The results suggest that scutellarin has a protective action against Con A-induced liver injury in mice, and its active mechanism may be related to the inhibition of the NF-kappaB-TNF-alpha-iNOS transduction pathway.     

The cyclo-oxygenase-2 inhibitor, rofecoxib, attenuates mucosal damage due to colitis induced by trinitrobenzene sulphonic acid in rats

Cyclo-oxygenase-2 overexpression has been described in experimental colitis. However, there are controversial findings suggesting that its inhibition by selective cyclo-oxygenase-2 inhibitors not only may have a beneficial effect on experimental colitis, but also exacerbate the inflammation-associated colonic injury. Thus, the role of cyclo-oxygenase-2 inhibitors in the possible modulation of colon inflammation is controversial and remains uncertain. In this study, we evaluated the effects of the selective cyclo-oxygenase-2 inhibitor, rofecoxib, on the extent and severity of ulcerative colitis caused by intracolonic administration of 2,4,6-trinitrobenzene sulphonic acid (TNBS) in rats. The lesions and the inflammatory response were assessed by histology and measurement of myeloperoxidase activity. Interleukin-1 beta, prostaglandin E(2) and D(2) levels in colon mucosa and the immunohistochemical expression of the cyclo-oxygenases-1 and -2 were also studied. Finally, we investigated the effects of rofecoxib on apoptosis of colonocytes by the appearance of DNA fragmentation. Inflammation following TNBS was characterized by increased colonic wall thickness, oedema, diffuse inflammatory cell infiltration in the mucosa, and necrosis. Increased myeloperoxidase activity, as an index of neutrophil infiltration in the mucosa, and interleukin-1 beta levels were also measured in the colon. Administration of rofecoxib significantly (P<0.05) reduced the colonic damage, the degree of neutrophil infiltration, and interleukin-1 beta levels. In addition, apoptosis was significantly increased in TNBS-treated rats, but not in rofecoxib plus TNBS-treated rats. We concluded that rofecoxib seems to have beneficial effects in TNBS-induced colitis by diminishing the initial stage of inflammation, probably by a mechanism related to inhibition of prostaglandin E(2) by the cyclo-oxygenase-2 pathway. The data suggest that cyclo-oxygenase-2-selective inhibitors may have a therapeutic role in ulcerative colitis.     

The protective effect of syringic acid on dextran sulfate sodium-induced experimental colitis in BALB/c mice

Inflammatory bowel diseases involve chronic intestinal inflammation which is mostly caused by Crohn's disease and ulcerative colitis (UC) conditions. Patients having UC are prone to colorectal cancer and dysplastic polyps, and also have sporadic adenomas. Syringic acid (SA) possesses many health benefits including antioxidant, anti-bacterial, and anti-cancer. This study was aimed to identify the effects of SA on UC, using a murine experimental model. Clinical symptoms and weight loss were significantly reduced in mice induced with dextran sulfate sodium (DSS) and treated with SA, compared to untreated mice. The effects of SA exhibited in DSS-induced mice were associated with significant decrease in the expressions levels of inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), pro-inflammatory cytokines (tumor necrosis factor [TNF-α], interleukin [IL-1β and IL-6]), remarkable amelioration of colonic architectural disruption, and a significant reduction in the activity of colonic myeloperoxidase. To further confirm the anti-inflammatory property of SA, RAW 264.7 cells were stimulated with lipopolysaccharides. SA dose-dependently inhibited the cytokines TNF-α, IL-1β, and IL-6. It also decreased the expressions of p65-NF-κB and IκB, thus reducing the activation and nuclear accumulation of p-STAT-3^Y705. This prohibited the degradation of inhibitory protein, IκB, as well as inhibited the nuclear translocation of p65-NF-κB in colonic tissue. It was concluded that SA has a potential to limit inflammation via inhibiting the p65-NF-κB and STAT3 signaling; hence it can be used for therapeutic purposes.     

Protective effect of marine mangrove Rhizophora apiculata on acetic acid induced experimental colitis by regulating anti-oxidant enzymes,inflammatory mediators and nuclear factor-kappa B subunits

Ulcerative colitis is a disease that causes inflammation and ulcer in the lining of the large intestine. In this study we investigate the effect of Rhizophora apiculata (R. apiculata) on acetic acid induced colitis in mouse model. Experimental animals were randomized into four groups: normal untreated, colitis control, R. apiculata treated group and sulfasalazine treated group. R. apiculata significantly (p < 0.01) decreased macroscopic score and wet weight of damaged colon compared to colitis control. This effect was confirmed biochemically by significant (p < 0.01) reduction of colitis associated increase in myeloperoxidase activity. R. apiculata significantly (p < 0.05) increased anti-oxidant enzymes such as superoxide dismutase (SOD) and glutathione (GSH) levels compared to colitis control. R. apiculata significantly (p < 0.01) reduced lipid peroxides (LPO), nitric oxide (NO) and inflammatory mediators such as myeloperoxidase (MPO), lactate dehydrogenase (LDH), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and tumor necrosis factor-α (TNF-α) expressions compared to colitis control. R. apiculata treatment significantly (p < 0.01) inhibits the translocation of NF-kB p65 and p50 subunits. Taken together these findings suggest that R. apiculata prevents acetic acid induced colitis in experimental mouse model and may serve as an excellent anti-oxidant and anti-inflammatory agent that could potentially be useful as a (natural) therapy for inflammatory bowel disease (IBD).     

Protective effect of taurohyodeoxycholic acid from Pulvis Fellis Suis on trinitrobenzene sulfonic acid induced ulcerative colitis in mice

Ulcerative colitis is a nonspecific inflammatory disorder characterized by oxidative and nitrosative stress, leucocyte infiltration and up-regulation of pro-inflammatory cytokines. The aim of this study is to evaluate the effect of taurohyodeoxycholic acid (THDCA) isolated from Pulvis Fellis Suis on acute ulcerative colitis model induced by trinitrobenzene sulfonic acid (TNBS) in mice. The efficacy of THDCA was studied by macroscopical and histological scoring systems as well as myeloperoxidase (MPO) activity. Serum levels, including tumor necrosis factor (TNF)-α and interleukin (IL)-6 were assayed by enzyme-linked immunoassay. The expression of cyclooxygenase (COX)-2 in the colons was assessed by immunohistochemical analysis. Treatment with THDCA in doses of 25, 50 and 100 mg/kg/day and sulfasalazine in a dose of 500 mg/kg/day used as reference for 7 consecutive days after the induction of colitis, significantly decreased colonic MPO activity, TNF-α, IL-6 serum levels and the expression of COX-2 in colon compared with TNBS induced ulcerative colitis model group. Moreover, THDCA attenuated the macroscopic colonic damage and the histopathological changes induced by TNBS. All the effects of these parameters were comparable to that of the standard sulfasalazine, especially at the highest dose level. The results suggested that THDCA from Pulvis Fellis Suis has a protective effect in TNBS-induced ulcerative colitis which might be due to its anti-inflammatory activities, and that it may have therapeutic value in the setting of inflammatory bowel disease.     

Protective effects of betulinic acid on intestinal mucosal injury induced by cyclophosphamide in mice

BackgroundBetulinic acid (BA) is a plant-derived pentacyclic triterpenoid with a variety of biological activities. The purpose of this study was to assess the potential protective role of BA against intestinal mucosal injury induced by cyclophosphamide (CYP) treatment.MethodsMice were pretreated with BA daily (0.05, 0.5, and 5.0 mg/kg) for 14 days, then injected intraperitoneally with CYP (50 mg/kg) for 2 days.ResultsBA pretreatment reduced the contents of malondialdehyde (MDA) and glutathione (GSH), decreased the activity of superoxide dismutase (SOD) in small intestine, increased villus hight/crypt depth ratio and restored the morphology of intestinal villi in CYP-induced mice. Moreover, BA pretreatment could significantly down-regulate the levels of pro-inflammatory cytokines interleukin-5 (IL-5), IL-17, IL-12 (P70) and tumor necrosis factor α (TNF-α), reduced production of chemokines macrophage inflammatory protein-1α (MIP-1α), macrophage inflammatory protein-1β (MIP-1β) and regulated upon activation, normal T-cell expressed and secreted (RANTES), and enhanced the levels of anti-inflammatory such as IL-2 and IL-10 in serum, and decreased the mRNA expressions of IL-1β and TNF-α in intestine of CYP-induced mice. Furthermore, RT-PCR demonstrated that BA improved intestinal physical and immunological barrier in CYP-stimulated mice by enhancing the mRNA expressions of zonula occluden 1 (ZO-1) and Claudin-1.ConclusionsBA might be considered as an effective agent in the amelioration of the intestinal mucosal resulting from CYP treatment.     

槲皮素等对烫伤后小鼠肠粘膜损伤的保护作用

目的　研究槲皮素、芸香苷、黄色素母酮 3种黄酮类化合物对烫伤所致小鼠肠粘膜损伤的保护作用。方法　观察小肠肠粘膜损伤指数的变化 ,检测肠粘膜中蛋白质、DNA含量变化 ,DTNB法测定肠粘膜中GSH的含量 ,并应用DNA解旋的荧光检测法测定DNA损伤程度。结果　槲皮素等三种黄酮类化合物连续 3d灌胃可不同程度的改善烫伤所致肠粘膜损伤状况 ,使肠粘膜损伤指数降低 ,蛋白质、DNA、GSH含量增加 ,DNA损伤程度减轻。其中尤以槲皮素作用较为明显。结论　槲皮素、芸香苷、黄色素母酮 3种黄酮类化合物可明显改善烫伤所致小鼠肠粘膜损伤 ,其机制可能与其抗氧化作用有关。     

Anti-inflammatory effect of kaurenoic acid, a diterpene from Copaifera langsdorffi on acetic acid-induced colitis in rats

Kaurenoic acid, a diterpene from Copaifera langsdorffii (Leguminaceae), was evaluated on rat colitis induced by acetic acid. Rats were pretreated orally (15 and 2 h before) or rectally 2 h before induction of colitis with kaurenoic acid (50 and 100 mg/kg) or vehicle (1 ml, 3% DMSO). Colitis was induced by intracolonic instillation of a 2 ml of 4% (v/v) acetic acid solution and, 24 h later, the colonic mucosal damage was analysed macroscopically for the severity of mucosal damage, the myeloperoxidase (MPO) activity and the malondialdehyde (MDA) levels in the colon segments. A marked reduction in gross damage score (52% and 42%) and wet weight of damaged colon tissue (39% and 32%) were observed in rats that received 100 mg/kg kaurenoic acid, respectively, by rectal and oral routes. This effect was confirmed biochemically by a two- to three-fold reduction of colitis associated increase in MPO activity, the marker of neutrophilic infiltration and by a marked decrease in MDA level, an indicator of lipoperoxidation in colon tissue. Furthermore, light microscopy revealed the marked diminution of inflammatory cell infiltration and submucosal edema formation in the colon segments of rats treated with the test compound. These findings indicate the anti-inflammatory potential of kaurenoic acid in acetic acid-induced colitis.     

Inhibitory effect of baicalein on mice tremor induced by oxotremorine and mechanisms

OBJECTIVE To investigate the anti-tremor effect and mechanism of baicalein on oxotremorine-induced muscle tremor in mice.METHODS The acute model of muscular tremor was induced by intraperitoneal injection of oxotremorine,and the latency,duration and frequency of muscle tremor in mice were measured immediately;the saliva of mice was measured to reflect the correlation between tremor and peripheral nerve function;the aim of this study was to determine the content of MDA and the activity of GSH-PX,and to investigate the anti-oxidation of mice with tremor model.The activity of acetylcholinesterase(AchE)and acetylcholine transferase(ChA T)can indirectly reflect the level of acetylcholine in the brain.The level of monoamine neurotransmitters in brain tissue was determined by high performance liquid chromatography(HPLC-ECD).RESULTS The animals in the model group appeared obvious tremoring,salivating and erecting and other symptoms.Compared to the model group,there was no obvious inhibitory effect on the administration of each dose.After 7,14,21 and 28 d of continuous administration,the latency,duration and tremor frequency of tremor mice were significantly shortened,the levels of acetylcholine were significantly decreased,the changes of DOPAC and DA neurotransmitters in the brain of model group were recovered,regulate the dynamic balance of acetylcholine and dopamine in the brain.CONCLUSION Long-term administration can improve the tremor behavior of mice,the mechanismmay be related to the regulation of neurotransmittersin brain.     

Protective effect of butyrate against ethanol-induced gastric ulcers in mice by promoting the anti-inflammatory,anti-oxidant and mucosal defense mechanisms

Gastric ulcers (GUs) are a common type of peptic ulcer. Alcohol overdose is one of the main causes of GU, which is difficult to prevent. Although the protective effect of butyrate on inflammation-related diseases is well understood, its effect on GUs has not been reported. We investigated the protective effects of butyrate against ethanol-induced lesions to the gastric mucosa in mice and the underlying mechanisms. BALB/c mice were orally pretreated with butyrate for 30 min prior to the establishment of the GU model by challenge with absolute ethanol. Ethanol administration produced apparent mucosal injuries with morphological and histological damage, whereas butyrate pretreatment reduced the gastric mucosal injuries in a dose-dependent manner. Butyrate pretreatment also significantly ameliorated contents of malondialdehyde (MDA) and carbonyl proteins, and decreased levels of IL-1β, TNF-α and IL-6. The Western blot results consistently demonstrated that butyrate pretreatment attenuated the phosphorylation of NF-κB p65, p38 MAPK and ERKs in the gastric tissues. Additionally, gastric wall mucus (GWM), a parameter reflecting mucosal defense, was clearly increased by butyrate pretreatment. Butyrate pretreatment protects the gastric mucosa against ethanol-induced lesions by strengthening the mucosal defense and anti-oxidant and anti-inflammatory activities. As a necessary substance for the body, butyrate may be applied to the prevention and treatment of GUs.