| 龚宇,杨文健,李鸣一.毛兰素通过 JNK/c-Jun信号通路对 2型糖尿病大鼠肝脏损伤的保护作用机制研究[J].安徽医药,2023,27(4):663-668. |
| 毛兰素通过 JNK/c-Jun信号通路对 2型糖尿病大鼠肝脏损伤的保护作用机制研究 |
| Study on the protective mechanism of Erianin on liver injury in type 2 diabetic rats through the JNK/c-Jun signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2023.04.007 |
| 中文关键词: 毛兰素 糖尿病 原癌基因蛋白质 c-jun 肝脏损伤 c-Jun氨基末端激酶 氧化应激 大鼠， Sprague-Dawley |
| 英文关键词: Erianin Diabetes Proto-oncogene proteins c-jun Liver damage c-Jun N-terminal kinase Oxidative stress Rat, Sprague-Dawley |
| 基金项目:湖北医药学院资助项目( 23) |
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| 中文摘要: |
| 目的基于 c-Jun氨基末端激酶( JNK)/c-Jun信号通路对氧化应激反应的调控作用，研究毛兰素对 2型糖尿病大鼠肝脏损伤的保护作用。方法于 2021年 10月至 2022年 2月腹腔注射链脲佐菌素构建糖尿病大鼠模型，将造模成功大鼠分为模型组、毛兰素低剂量组( 10 mg/kg)、毛兰素高剂量组( 40 mg/kg)及罗格列酮组( 1.25 mg/kg)、毛兰素( 40 mg/kg)+JNK激活组(5 mg/ kg)，每组 10只，另取正常饲养大鼠 10只作为对照组。连续给药，6周后，通过血糖仪和胰岛素放射免疫分析试剂盒检测空腹血糖( FBG)、空腹胰岛素( FINS)水平，计算胰岛素抵抗指数( HOMA-IR)及胰岛素敏感指数( ISI)；天平称取大鼠体质量和肝质量，计算肝脏指数；试剂盒检测丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶( AST)、总超氧化物歧化酶( T-SOD)、谷胱甘肽过氧化物酶( GSH-Px)活性及丙二醛(MDA)含量； HE染色观察肝脏组织病理学变化； western blotting法检测肝脏组织中 JNK/c-Jun信号通路相关蛋白表达。结果与对照组相比，模型组肝脏指数［( 4.26±0.12)g/100 g比( 2.24±0.09)g/100 g］、 FBG［( 21.49±1.78)mmol/L比( 5.14±0.45)mmol/L］、 FINS［( 80.17±6.38)mmol/L比( 22.35±2.04)mmol/L］、 HOMA-IR［( 76.46±6.56)比( 5.11±1.12)］、 ALT［( 138.71±10.21)U/L比( 70.29±5.54)U/L］和 AST活性［( 77.21±5.08)U/L比( 40.38±3.27)U/L］、 MDA含量［( 13.45±1.34)nmol/mg prot比( 3.72±0.87)nmol/mg prot］、 JNK/c-Jun信号通路相关蛋白表达均明显升高( P<0.05)，体质量、 ISI［( ?7.45±0.18)比( ?4.74±0.11)］、 SOD［( 100.79±11.22)U/mg prot比( 223.46±19.86)U/mg prot］和 GSH-Px活性［( 24.42±1.74)U/mg prot比(56.79±3.18)U/mg prot］明显降低( P<0.05)，且肝脏组织病理损伤较为严重；与模型组相比，毛兰素低剂量组、毛兰素高剂量组和罗格列酮组肝脏指数、 FBG、FINS、HOMA-IR、ALT和 AST活性、 MDA含量、 JNK/c-Jun信号通路相关蛋白表达均明显降低( P<0.05)，体质量、 ISI、SOD和 GSH-Px活性明显升高( P<0.05)减轻肝脏损伤程度；与毛兰素高剂量组相比，毛兰素低剂量组、毛兰素+JNK激活组肝脏指数、 FBG、FINS、HOMA-IR、ALT和 AST活性、 MDA含量、 JNK/c-Jun信号通路相关蛋白表达均明显升高(P<0.05)体质量、 ISI、SOD和 GSH-Px活性明显降低( P<0.05)，肝脏损伤恢复缓慢。结论毛兰素可通过调控 JNK/c-Jun信号通路，抑制，JNK/c-Jun通路蛋白表达，从而缓解氧化应激反应，改善糖尿病大鼠肝脏损伤。 |
| 英文摘要: |
| Objective Based on the regulatory effect of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway on the oxidative stress response, we studied the protective effect of Erianin on liver injury in type 2 diabetic rats.Methods The diabetic rat model was constructed by intraperitoneal injection of streptozotocin from October 2021 to February 2022, and the successfully modeled rats were dividedinto the model group, Erianin low-dose group (10 mg/kg), Erianin high-dose group (40 mg/kg), rosiglitazone group (1.25 mg/kg), and Erianin (40 mg/kg) + JNK activator (5 mg/kg) group, with 10 rats in each group. After 6 weeks of continuous administration, the levels of fasting blood glucose (FBG) and fasting insulin (FINS) were detected by a glucose meter and insulin radioimmunoassay kit, and the insulin resistance index (HOMA-IR) and insulin sensitivity index (ISI) were calculated; the body weight and liver weight of rats were weighed with abalance, and the liver index was calculated; the kit was used to detect the contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). HE staining was used toobserve the pathological changes in the liver. Western Blotting was used to detect the expression of JNK/c-Jun signaling pathway-related proteins in liver tissues. Results Compared with the control group, the liver index [(4.26±0.12) g/100 g vs. (2.24±0.09) g/100 g], FBG [(21.49±1.78) mmol/L vs. (5.14±0.45) mmol/L], FINS [(80.17±6.38) mmol/L vs. (22.35±2.04) mmol/L], HOMA-IR [(76.46±6.56) vs. (5.11± 1.12)], ALT [(138.71±10.21) U/L vs. (70.29±5.54) U/L] and AST activity [(77.21±5.08) U/L vs. (40.38±3.27) U/L], and MDA content [(13.45±1.34) nmol/mg prot vs. (3.72±0.87) nmol/mg prot], and JNK/c-Jun signaling pathway-related protein expression in the model group were significantly higher (P < 0.05), the body weight, ISI [(?7.45±0.18) vs. (?4.74±0.11)], SOD [(100.79±11.22) U/mg prot vs. (223.46± 19.86) U/mg prot] and GSH-Px activity [(24.42±1.74) U/mg prot vs.(56.79±3.18) U/mg prot] were significantly lower (P < 0.05), and liver tissue pathological damage was more severe. Compared with the model group, the liver index, FBG, FINS, HOMA-IR, ALT and AST activities, MDA content, and JNK/c-Jun signaling pathway-related protein expression in the Erianin low-dose group, Erianin high-dose group, and rosiglitazone group were significantly lower (P < 0.05), and the body weight, ISI, SOD and GSH-Px activities were significantly higher (P < 0.05), reducing the degree of liver injury. Compared with the Erianin high-dose group, the liver index, FBG, FINS, HOMA-IR, ALT and AST activities, MDA content, and JNK/c-Jun signaling pathway-related protein expression in the Erianin low dose group and Erianin + JNK activator group were significantly higher (P < 0.05), the body weight, ISI, SOD and GSH-Px activities were significantly lower (P < 0.05), and slow recovery from liver injury was observed.Conclusion Erianin ameliorates oxidative stress and improves liver injury in diabetic rats by regulating the JNK/c-Jun signaling pathway and inhibiting the JNK/c-Jun pathway protein expression. |
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