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孙惠萍,王剑,张小芳.五味子乙素通过抑制NF-κB/ COX-2活化来抑制CCl 4诱导的肝损伤[J].浙江中西医结合杂志,2021,31(6):
五味子乙素通过抑制NF-κB/ COX-2活化来抑制CCl 4诱导的肝损伤
Schizandrin B inhibits CCl 4 induced liver injury by inhibiting NF-κB/COX-2 activation
投稿时间:2020-11-20  修订日期:2021-04-23
DOI:
中文关键词:  肝损伤  五味子乙素  NF-κB  COX-2  抗氧化
英文关键词:liver injury  schisandrin B  NF-κB  COX-2  antioxidant
基金项目:
作者单位E-mail
孙惠萍 浙江省荣军医院 sunhuiping011@163.com 
王剑 浙江省荣军医院药剂科  
张小芳 浙江省荣军医院药剂科  
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中文摘要:
      目的:探讨五味子乙素对CCl 4诱导的肝损伤的影响及其可能机制。方法:不同浓度五味子乙素处理HepG2细胞,CCK-8测定细胞活力,DPPH自由基清除活性测量五味子乙素的抗氧化活性。18只Wistar大鼠根据随机数字表法分为对照组、模型组和五味子乙素组,腹腔注射20%CCl4(2 mL / kg)诱导肝损伤,五味子乙素组以50 mg / kg 五味子乙素灌胃,对照组灌胃等量0.9%氯化钠溶液,检测血清碱性磷酸酶(ALP)、天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT),苏木精-伊红(HE)染色进行组织学分析,蛋白印迹检测肝组织和肝癌细胞NF-κB和COX-2的蛋白表达。结果:五味子乙素的抗氧化活性随浓度的增加而增加[50、100、150和200 μM 五味子乙素的DPPH自由基清除率分别为(72.29±0.54)%、(82.81±0.45)%、(91.74±0.98)%和(98.63±1.15)%,P<0.05],以剂量依赖性方式降低了HepG2细胞的活力[5、10、20、40和80μM 五味子乙素的细胞活力分别为(94.81±3.07) %、(88.21±3.67) %、(78.09±5.73) %、(59.23±13.35) %和(27.57±13.94) %,P<0.05]。与模型组相比,五味子乙素组体重[(297.89±13.47)g比(374.31±15.77)g]显著升高,肝脏重量[(14.84±1.73)g比(12.72±1.18)g]和肝指数(0.05±0.007比0.03±0.002)显著降低(P<0.05)。五味子乙素组ALP[(630.81±53.71)U/L比(146.42±6.48)U/L]、AST[(143.05±13.60)U/L比(69.92±8.49) U/L]和ALT[(153.82±16.34)U/L比(47.81±9.97)U/L]较模型组均显著降低(P<0.05),五味子乙素处理可明显减轻CCl 4引起的肝组织损害,五味子乙素处理可在体内和体外抑制NF-κB和COX-2的活化(P<0.05)。结论:五味子乙素可能通过抑制NF-κB/ COX-2活化来抑制CCl 4诱导的肝损伤。
英文摘要:
      Objective: To investigate the effect of Schisandrin B on liver injury induced by CCl 4 and its possible mechanism. Method: HepG2 cells were treated with different concentrations of Schisandrin B, cell viability was measured by CCK-8, and the antioxidant activity of Schisandrin B was measured by using DPPH free radical scavenging activity. Eighteen Wistar rats were randomly divided into Control group, Model group and Schisandrin B group. Intraperitoneal injection of 20% CCl4 (2 mL/kg) induced liver injury. Schisandrin B group received 50 mg/kg Schisandrin B was intragastrically administered, and the control group was intragastrically administered with the same amount of 0.9% sodium chloride solution to detect serum alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and HE staining for tissue Scientific analysis, western blotting to detect protein expression of NF-κB and COX-2 in liver tissue and liver cancer cells. Results: The antioxidant activity of Schisandrin B increased with the increase in concentration[The DPPH free radical scavenging rates of 50, 100, 150 and 200 μM Schisandrin B were (72.29±0.54)%, (82.81±0.45)%, (91.74±0.98)% and (98.63±1.15)%, respectively, P< 0.05], and decreased the viability of HepG2 cells in a dose-dependent manner[The cell viability of 5, 10, 20, 40 and 80μM Schisandrin B were (94.81±3.07)%, (88.21±3.67)%, (78.09±5.73)%, (59.23±13.35)% and (27.57±13.94) %, respectively, P<0.05]. Compared with the Model group, the body weight [(297.89±13.47)g vs (374.31±15.77)g] of the Schisandrin B group was significantly increased, and the liver weight [(14.84±1.73)g vs (12.72±1.18)g] and liver index (0.05±0.007 vs 0.03±0.002) were significantly reduced (P<0.05). ALP [(630.81±53.71)U/L vs (146.42±6.48)U/L], AST [(143.05±13.60)U/L vs (69.92±8.49) U/L] and ALT [(153.82±16.34)U/L vs (47.81±9.97)U/L] of Schisandrin B group were significantly lower than those of Model group (P<0.05). Schisandrin B treatment can significantly reduce liver damage caused by CCl 4, and Schisandrin B treatment can inhibit NF-κB in vivo and in vitro And COX-2 activation (P<0.05). Conclusion: Schizandrin B may inhibit CCl 4 induced liver injury by inhibiting NF-κB/COX-2 activation.
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