舒广文,邱韵涵,付千,段欢,余惠凡,邓旭坤.桑葚总多糖对对乙酰氨基酚诱导小鼠急性肝损伤的保护作用[J].中南民族大学学报自然科学版,2019,(3):377-382
桑葚总多糖对对乙酰氨基酚诱导小鼠急性肝损伤的保护作用
Alleviation effects of total polysaccharides from fruits of Morus alba L. on acetaminophen-induced acute liver injury in mice
  
DOI:10.12130/znmdzk.20190311
中文关键词: 桑葚总多糖  肝损伤  抗氧化  抗炎
英文关键词: total polysaccharides of Morus alba L.  liver injury  anti-oxidation  anti-inflammation
基金项目:湖北省自然科学基金资助项目(2018CFB624);中南民族大学2018年硕士研究生学术创新基金项目(2018sycxjj223)
作者单位
舒广文,邱韵涵,付千,段欢,余惠凡,邓旭坤 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
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中文摘要:
      目的:研究桑葚总多糖(MFP) APAP对HepG2肝细胞毒性的缓解效应,探讨MFP对APAP诱导小鼠急性肝损伤的保护作用及可能机制.方法:采用MTT法检测MFP对细胞活力的影响,将32只小鼠随机分为正常组、模型组、MFP低、高剂量组(50, 150 mg/kg),腹腔注射300 mg/kg APAP建立小鼠急性肝损伤模型,检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)和乳酸脱氢酶(LDH)活力,肝组织中丙二醛(MDA)、还原型谷胱甘肽(GSH)、总超氧化物歧化酶(T-SOD)和总抗氧化能力(T-AOC)水平;用EILISA测定肝组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)水平;HE染色法观察肝脏组织的病理学变化;用Western blot检测小鼠肝组织中核因子-kB(NF-kB)p65、血红素加氧酶(HO-1)和葡萄糖-6-磷酸脱氢酶(G6PD)的表达水平.结果:MFP可剂量依赖性地缓解APAP诱导的HepG2细胞死亡(P<0.01).与模型组相比,MFP能显著地降低肝损伤小鼠血清中ALT, AST, LDH水平(P<0.05或P<0.01),下调肝组织中MDA, TNF-α, IL-1β, IL-6的含量(P<0.05或P<0.01),改善APAP诱导的小鼠肝组织病变.此外,MFP还能明显上调模型小鼠肝组织中GSH, T-SOD, T-AOC水平(P<0.05或P<0.01),明显下调NF-kB p65蛋白的表达水平(P<0.05或P<0.01),上调HO-1和G6PD蛋白的表达水平(P<0.05或P<0.01).结论:MFP能保护APAP诱导的小鼠急性肝损伤,这与增强肝脏抗氧化能力,抑制肝脏炎症反应有关.
英文摘要:
      Objective: To study the alleviation effect of mulberry total polysaccharide (MFP) APAP on HepG2 hepatocyte toxicity, and to explore the protective effect and possible mechanism of MFP on APAP-induced acute liver injury in mice. Methods: MTT assay was used to detect the effect of MFP on cell viability. 32 mice were randomly divided into normal group, model group, MFP low and high dose group (50, 150 mg/kg), and acute liver injury mice model were established by intraperitoneal injection of 300 mg/kg APAP. Serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), and hepatic levels of malondialdehyde (MDA), glutathione (GSH), total superoxide dismutase (T-SOD), and total antioxidant capacity (T-AOC) were determined. Levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the livers were also detected. The pathological changes of liver tissue was observed by HE staining , and protein expression levels of nuclear factor-kB (NF-kB) p65, hemeoxygenase-1 (HO-1) and glucose-6-phosphate dehydrogenase (G6PD) were detected by Western blot. Results: MFP dose-dependently alleviated APAP-induced HepG2 cell death(P<0.01). Compared with the model group, MFP significantly declined levels of ALT, AST, and LDH in serum(P<0.05, P<0.01), reduced hepatic contents of MDA, TNF-α, IL-1β and IL-6(P<0.05, P<0.01), and ameliorated liver histopathological changes provoked by APAP. Moreover, MFP markedly elevated levels of GSH, T-SOD and T-AOC(P<0.05, P<0.01), decreased protein expressions of NF-kB p65(P<0.05, P<0.01), and up-regulated those of HO-1 and G6PD(P<0.05, P<0.01). Conclusion: MFP can alleviate APAP-induced acute liver injury in mice, which is related to enhancement of the antioxidation and inflammation inhibition capacity of liver.
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