Protective effect of l -citrulline against ethanol-induced gastric ulcer in rats

Liu, Yi; Xia, Tian; Gou, Lingshan; Fu, Xiangyu; Li, Sai; Lan, Nuo; Yin, Xiaoxing

doi:10.1016/j.etap.2012.04.009

Cited by 82 publications

(77 citation statements)

References 34 publications

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“…However, we found that L-citrulline has an improvement in renal cell energy metabolism facilitates the repair of oxidized membrane/ Lipid bilayers and the phenomenon of functional, biochemical, and morphological renal impairment which connected to the lipid peroxidation was prevented by the antioxidant effect. Also, L-citrulline activity as a direct ROS scavenger has been reported, 19 and it could indirectly increase in the intracellular GSH and SOD in the rat kidney tissues.…”

Section: Discussionmentioning

confidence: 99%

“…19 SOD evaluation was based on the generation of superoxide radicals produced by xanthine and xanthine oxidase, which reacted with nitro-blue tetrazolium (NTB) to form formazan dye. SOD activity was then read at 550 nm by the degree of inhibition of this reaction.…”

Section: Sod Activitymentioning

confidence: 99%

“…16 Others demonstrated that oral supplementation of L-citrulline can inhibition the increased inducible nitric oxide synthase (iNOS) activity, upregulate endothelial NO synthase (eNOS) activity, and improve endothelial function in animal. [17][18][19] The purpose of this present study was to evaluate the protective effects of L-citrulline supplementation on the glycerol-induced ARF in rats, and its underlying mechanism.…”

Section: Introductionmentioning

confidence: 99%

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L-Citrulline Protects Against Glycerol-Induced Acute Renal Failure in Rats

Liu

Gou

et al. 2013

Renal Failure

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There is an increasing evidence that oxidative stress plays an important role in the pathogenesis of rhabdomyolysisinduced acute renal failure (ARF). In this study, protective effects of L-citrulline on glycerol-induced ARF in rats were investigated. Six groups of rats were employed in this study: group 1 served as a control; group 2 was only given glycerol (50%, 10 mL/kg, i.m.); group 3 was given glycerol plus dexamethasone (0.1 mg/kg, i.g.) as positive reference drug, starting at the same time as the glycerol injections; the last three groups were given glycerol plus L-citrulline (300, 600, and 900 mg/kg, i.g.) respectively, starting at the same time as the glycerol injections. The injections of glycerol were only once, and after glycerol injections the i.g. administrations of dexamethasone and L-citrulline were repeated every 24 h for 7 days. After 7 days of glycerol injections, the blood samples and kidney tissues were harvested for future biochemical and pathology analyses. The levels of creatinine (Cr) and urea nitrogen (BUN) in plasma, the content of malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), the activity of total nitric oxide synthase (TNOS), inducible nitric oxide synthase (iNOS), endothelial NO synthase (eNOS), and superoxide dismutase (SOD) were evaluated in kidney tissues. Consequently, administrations of L-citrulline improved an impaired intrarenal oxygenation and kidney function compared with the glycerol group, and prevented the renal oxidative stress damage as well as severe functional and morphological renal deterioration. Therefore, L-citrulline might have potential application in the amelioration of glycerol-induced ARF.

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Section: Discussionmentioning

confidence: 99%

Section: Sod Activitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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L-Citrulline Protects Against Glycerol-Induced Acute Renal Failure in Rats

Liu

Gou

et al. 2013

Renal Failure

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“…The gastric mucosa is important tissue because of its structure and function, which can reflect the pathological processes by the inflammation changes of gastric ulcer 3 . The mucosal defense has been best characterized in the gastric, which exhibits remarkable resistance to the damaging effects of acid and pepsin 4 .…”

Section: Introductionmentioning

confidence: 99%

Therapeutic effect of low molecular weight chitosan containing sepia ink on ethanol-induced gastric ulcer in rats

Zhang

Liu

et al. 2016

Acta Cir. Bras.

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PURPOSE:To evaluate the role of low molecular chitosan containing sepia ink (LMCS) in ethanol-induced (5 ml/kg) gastric ulcer in rats. METHODS:Animals were divided into four groups (n = 12): normal group (Normal), negative control group (Con), experiment group (LMCS) and positive control Omeprazole group (OMZ). Gastric empty rate was detected in the first 7 days. Rats were sacrificed at 7, 14 and 21 day for histology and ELISA detections. RESULTS:Gastric empty was no significant differences among the groups (P > 0.05). Histological observation showed gastric mucosal LMCS treated had better healing effect. Hydroxyproline (Hyp) was significantly increased from 7 day (P < 0.05). LMCS significantly inhibited malondialdehyde (MDA) generation for lipid peroxidation from 7 day (P < 0.05). LMCS significantly promoted the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) at the earlier stage (P < 0.05). OMZ had the similar effects above. As for myeloperoxidase (MPO), LMCS significantly decreased and restored it to normal levels from 7 day (P < 0.05), it is earlier than OMZ which is from 14 day.CONCLUSION: LMCS can improve gastric mucosa tissue repair, exert significant influences on oxidative and antioxidant enzyme activities and neutrophil infiltration.

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“…These findings are in accordance with earlier reports as GSH levels were significantly depleted in gastric homogenate of rats, when exposed with ethanol. 35,36 Pretreatment of rats with sider honey replenished GSH level as compared with ethanl only treated animals, suggesting the ameliorative effects of sider honey. Moreover, ethanol was reported to induced lipid peroxidation in the gatric wall of induced animals.…”

Section: Resultsmentioning

confidence: 99%

Effectiveness of Sidr Honey on the prevention of ethanol-induced gatroulcerogenesis: role of antioxidant and antiapoptotic mechanism

Taha¹,

Abdelwahab²,

Elsanousi³

et al. 2015

Phcog J

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Background: Sider (Ziziphus spina-christi (L.) Desf.) Honey has been used for the treatment of gastrointestinal disorders including peptic ulcer. Aim of the study: The mechanism of the antiulcer effect of sider honey was studied placing emphasis on its role to block oxidative damage and apoptosis during ethanol-induced gastric ulceration in rats. The mechanism of the antiulcer effect of sider honey was studied placing emphasis on its role to block oxidative damage and apoptosis during ethanol-induced gastric ulceration in rats. Materials and methods: Experimental animals were orally treated with sidr honey (100, 250 and 500 mg/kg, respectively) or omeprazole and subsequently exposed to 95%ethanol (5 mL/Kg, orally) to induce acute gastroulcerogenesis. Effectiveness of sidr honey was evaluated using ulcer index, pH of gastric juice, mucus content, morphological analyses, glutathione assay and malondialdehyde level. The anti-apoptotic role of sidr honey was studied using immunohistochemical staining of gastric tissues using monoclonal antibodies of Bax pathway. Results: Dose-response studies in ethanol-induced ulcer indicate that sidr honey significantly blocks gastric lesions at lower dose (100 mg/kg). Lipid peroxidation and glutathione depletion were significantly inhibited by sidr honey. Sidr honey modulated the immuno-expression of mitochondrial associated protein (Bax). Conclusion: Thus, sider honey plays a considerable role in gastro protection by acting as a potent antioxidant and antiapoptotic agent. Future study is required to explore its potential clinical usage.

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Protective effect of l -citrulline against ethanol-induced gastric ulcer in rats

Cited by 82 publications

References 34 publications

L-Citrulline Protects Against Glycerol-Induced Acute Renal Failure in Rats

L-Citrulline Protects Against Glycerol-Induced Acute Renal Failure in Rats

Therapeutic effect of low molecular weight chitosan containing sepia ink on ethanol-induced gastric ulcer in rats

Effectiveness of Sidr Honey on the prevention of ethanol-induced gatroulcerogenesis: role of antioxidant and antiapoptotic mechanism

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