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喀什小檗提取物调控PPARγ/NF-κB信号通路对动脉粥样硬化模型大鼠氧化应激的影响

Effects of Kashgar Berberry Extract on Oxidative Stress in Atherosclerotic Rats through Regulating the PPARγ/NF-κB Signaling Pathway
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摘要 目的:观察喀什小檗提取物调控过氧化物酶体增殖物激活受体-γ(PPARγ)/核因子κB(NF-κB)信号通路对动脉粥样硬化模型大鼠氧化应激的影响。方法:55只无特定病原体(SPF)级雄性SD大鼠,取10只大鼠作为空白组,另外45只大鼠建立动脉粥样硬化模型,其中40只大鼠建模成功,将建模成功的40只大鼠随机分为模型组、阳性药物组、喀什小檗提取物低剂量组、喀什小檗提取物高剂量组,各10只。空白组、模型组给予生理盐水灌胃,阳性药物组给予阿托伐他汀灌胃,喀什小檗提取物低剂量组、高剂量组分别给予喀什小檗提取物60、240 mg/(kg·d)。观察各组大鼠主动脉组织病理组织学、氧化应激指标、血清血脂、内皮素-1(ET-1)、一氧化氮(NO)、PPARγmRNA、NF-κB mRNA表达量及PPARγ/NF-κB蛋白表达情况。结果:与空白组比较,模型组超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、高密度脂蛋白胆固醇(HDL-C)、NO、PPARγmRNA、PPARγ降低P<0.05),丙二醛(MDA)、活性氧(ROS)、低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)、三酰甘油(TG)、ET-1、NF-κB mRNA、NF-κB蛋白升高(P<0.05);与模型组比较,阳性药物组、喀什小檗提取物低剂量组、喀什小檗提取物高剂量组SOD、GSH-Px、HDL-C、NO、PPARγmRNA、PPARγ蛋白升高(P<0.05),MDA、ROS、LDL-C、TC、TG、ET-1、NF-κB mRNA、NF-κB蛋白降低(P<0.05);与阳性药物组比较,喀什小檗提取物低剂量组SOD、GSH-Px、HDL-C、NO、PPARγmRNA、PPARγ蛋白降低(P<0.05),MDA、ROS、LDL-C、TC、TG、ET-1、NF-κB mRNA、NF-κB蛋白升高,喀什小檗提取物高剂量组SOD、GSH-Px、LDL-C、TC、TG、NO、PPARγmRNA、PPARγ蛋白升高(P<0.05),MDA、ROS、HDL-C、ET-1、NF-κB mRNA、NF-κB蛋白降低(P<0.05)。结论:喀什小檗提取物可抑制动脉粥样硬化模型大鼠氧化应激反应,其作用机制可能与调控PPARγ/NF-κB信号通路有关。 Objective:To observe the effect of Kashgar Berberry Extract on the oxidative stress in atherosclerotic rat models by regulating the peroxisome proliferator-activated receptor-γ(PPARγ)/nuclear factorκB(NF-κB)signaling pathway.Methods:Fifty-five male SD rats of specific pathogen-free(SPF)grade were selected.Ten rats were set as the blank group,while the remaining 45 rats were used to establish the atherosclerosis model,with 40 rats successfully modeling the condition.Forty modeling rats were randomly divided into the model group,the positive drug group,the low-dose Kashgar Berberry Extract group,and the high-dose group,with 10 rats in each group.The blank group and the model group were gavaged with normal saline,the positive drug group was gavaged with atorvastatin,and the low-dose Kashgar Berberry Extract group,and the high-dose Kashgar Berberry Extract group were respectivelygavaged with 60 and 240 mg/(kg·d)of Kashgar Berberry Extract.The histopathological,oxidative stress,serum lipid,endothelin-1(ET-1),nitric oxide(NO),PPARγmRNA,NF-κB mRNA expressions,and PPARγ/NF-κB protein expression in the aortic tissues of each group of rats were observed.Results:Compared with the blank group,the levels of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),high-density lipoprotein cholesterol(HDL-C),NO,PPARγmRNA,and PPARγin the model group decreased(P<0.05),while malondialdehyde(MDA),reactive oxygen species(ROS),low-density lipoprotein cholesterol(LDL-C),total cholesterol(TC),triglycerides(TG),ET-1,NF-κB mRNA,and NF-κB increased(P<0.05).Compared with the model group,SOD,GSH-Px,HDL-C,NO,PPARγmRNA,and PPARγin the positive drug group,the low-dose Kashgar Berberry Extract group,and the high-dose group significantly increased(P<0.05),while MDA,ROS,LDL-C,TC,TG,ET-1,NF-κB mRNA,and NF-κB decreased(P<0.05).Compared with the positive drug group,SOD,GSH-Px,HDL-C,NO,PPARγmRNA,and PPARγin the low-dose Kashgar Berberry Extract group decreased(P<0.05),while MDA,ROS,LDL-C,TC,TG,ET-1,NF-κB mRNA,and NF-κB increased.SOD,GSH-Px,LDL-C,TC,TG,NO,PPARγmRNA,and PPARγin the high-dose Kashgar Berberry Extract group increased(P<0.05),while MDA,ROS,HDL-C,ET-1,NF-κB mRNA,and NF-κB decreased(P<0.05).Conclusion:Kashgar Berberry Extract group could improve the oxidative stress response in atherosclerotic model rats,while its mechanism might be related to regulate the PPARγ/NF-κB signaling pathway.
作者 张裕祥 桑国耀 何雪娇 宋建涛 ZHANG Yuxiang;SANG Guoyao;HE Xuejiao;SONG Jiantao(The Sixth Affiliated Hospital of Xinjiang Medical University,Urumqi 830002,Xinjiang,China;The First Affiliated Hospital of Xinjiang Medical University,Urumqi 830002,Xinjiang,China)
出处 《中西医结合心脑血管病杂志》 2026年第3期350-356,共7页 Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基金 新疆医科大学第六附属医院青年拔尖人才项目(No.LFYKYZXJJ2024002) 乌鲁木齐市卫生健康委员会科技计划项目(No.202504WSWJWKJCXTDFH)。
关键词 动脉粥样硬化 喀什小檗提取物 过氧化物酶体增殖物激活受体-Γ 核因子ΚB 氧化应激 实验研究 atherosclerosis Kashgar Berberry peroxisome proliferator-activated receptor-γ nuclear factorκB oxidative stress experimental study
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