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Effect of sodium butyrate on gastric ulcer aggravation and hepatic injury inflicted by bile duct ligation in rats.
Saudi Pharmaceutical Journal ( IF 4.1 ) Pub Date : 2020-04-25 , DOI: 10.1016/j.jsps.2020.04.008
Neveen A Elnozahi 1 , Esraa A Said 1 , Azza E Bistawroos 1 , Rania G Aly 2
Affiliation  

Background and Aim

Cholestasis is positively associated with an increased risk of peptic ulceration. The present study investigated the aggravating effect of cholestasis on piroxicam-induced gastric ulceration. The study also evaluated the effect of sodium butyrate (SoB) on piroxicam-induced gastric ulceration in cholestatic animals and its effect on hepatic tissues and both effects were compared to ursodeoxycholic acid (UDCA) as a standard anticholestatic drug.

Methods

Bile duct ligation was adopted for induction of cholestasis in rats. The cholestatic animals received saline, SoB (P.O, 400 mg/kg, twice daily) or UDCA (P.O, 30 mg/kg/day) for 4 days starting from the first day of surgery. On the 4th day, blood samples were collected for determination of serum hepatic markers, then gastric ulcers were induced by piroxicam administration (P.O, 50 mg/kg) and 4 h later, the stomach was isolated and gastric mucosa was collected for biochemical determinations. The ulcer indices for the investigated drugs were compared to omeprazole as a standard acid suppressive drug.

Results

Piroxicam-induced ulceration was exacerbated in cholestatic rats. Gastric mucosa showed a significant elevation of MDA and TNF-α together with a significant decrease in GSH &VEGF levels. SoB treatment significantly attenuated ulcer development. The afforded protection was higher than that provided by UDCA and was not significantly different from that afforded by omeprazole. SoB significantly decreased gastric mucosal MDA and TNF-α level, whereas UDCA failed to alter these parameters. Both drugs significantly elevated GSH, VEGF and IL10 levels. Similar to UDCA, SoB showed a significant reduction in AST, ALT, GGT, ALP and bilirubin level. Histopathological examination confirmed the attenuating effect of SoB on gastric and hepatic injury.

Conclusions

Sodium butyrate effectively protected gastric and hepatic tissues against cholestasis-induced damage. Gastroprotection was mediated through antioxidant, anti-inflammatory and angiogenic activities.



中文翻译:

丁酸钠对胆管结扎大鼠胃溃疡加重及肝损伤的影响

背景和目标

胆汁淤积与消化性溃疡风险增加呈正相关。本研究调查了胆汁淤积对吡罗昔康诱发的胃溃疡的加重作用。该研究还评估了丁酸钠(SoB)对胆汁淤积动物中吡罗昔康诱发的胃溃疡的作用及其对肝组织的影响,并将这两种作用与作为标准抗胆汁淤积药物的熊去氧胆酸(UDCA)进行了比较。

方法

采用胆管结扎诱导大鼠胆汁淤积。胆汁淤积动物从手术第一天开始连续4天接受盐水、SoB(PO,400 mg/kg,每天两次)或UDCA(PO,30 mg/kg/天)。第4天采血测定血清肝标志物,给予吡罗昔康(PO,50mg/kg)诱发胃溃疡,4h后离体胃,收集胃粘膜进行生化测定。将所研究药物的溃疡指数与作为标准抑酸药物的奥美拉唑进行比较。

结果

胆汁淤积大鼠中吡罗昔康诱发的溃疡加剧。胃粘膜显示 MDA 和 TNF-α 显着升高,同时 GSH 和 VEGF 水平显着降低。SoB 治疗显着减轻了溃疡的发展。所提供的保护高于 UDCA 所提供的保护,并且与奥美拉唑所提供的保护没有显着差异。SoB 显着降低胃粘膜 MDA 和 TNF-α 水平,而 UDCA 未能改变这些参数。两种药物均显着升高 GSH、VEGF 和 IL10 水平。与 UDCA 类似,SoB 显示 AST、ALT、GGT、ALP 和胆红素水平显着降低。组织病理学检查证实了 SoB 对胃和肝损伤的减轻作用。

结论

丁酸钠有效保护胃和肝组织免受胆汁淤积引起的损伤。胃保护是通过抗氧化、抗炎和血管生成活性介导的。

更新日期:2020-04-25
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