血脂康通过AMPK/eNOS对糖尿病肾病大鼠的肾脏保护作用OA
Reno protective effect of Xuezhikang in diabetic kidney disease rats via AMPK/eNOS
目的 研究血脂康通过腺苷酸蛋白活化激酶(AMPK)/内皮型一氧化氮合酶(eNOS)通路对糖尿病肾病(DKD)大鼠的肾脏保护作用.方法 将SD大鼠随机分为对照组、模型组(建立DKD模型)、血脂康组(DKD建模及1 200 mg/(kg·d)血脂康灌胃)、抑制剂组(DKD建模及0.2 mg/(kg·d)AMPK抑制剂Compound C腹腔注射)、血脂康+抑制剂组(DKD建模及1 200 mg/(kg·d)血脂康灌胃、0.2 mg/(kg·d)AMPK抑制剂Compound C腹腔注射).干预4周后检测大鼠肾脏病理变化、肾功能指标(24 h尿白蛋白、血肌酐(Scr)、血尿素氮(BUN))、肾脏中磷酸化AMPK(p-AMPK)及eNOS表达水平、炎症指标(肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6))、氧化应激指标(超氧化物歧化酶(SOD)、丙二醛(MDA))表达水平.结果 与模型组比较,血脂康组的肾脏病理损伤减轻,24 h尿白蛋白、Scr、BUN及肾脏中TNF-α、IL-6、MDA水平降低,肾脏中p-AMPK、eNOS表达水平及SOD水平增加(P<0.05);抑制剂组的肾脏病理改变加重,24 h尿白蛋白、Scr、BUN及肾脏中TNF-α、IL-6、MDA水平增加,肾脏中p-AMPK、eNOS表达水平及SOD水平降低(P<0.05).与血脂康组比较,血脂康+抑制剂组的肾脏病理改变加重,24 h尿白蛋白、Scr、BUN及肾脏中TNF-α、IL-6、MDA水平增加,肾脏中p-AMPK、eNOS表达水平及SOD水平降低(P<0.05).结论 血脂康通过激活AMPK/eNOS减轻DKD大鼠肾脏损伤及炎症反应、氧化应激反应.
Objective To investigate the renoprotective effect of Xuezhikang in rats with diabetic kidney disease(DKD),via AMP-activated protein kinase(AMPK)/endothelial nitric oxide synthase(eNOS)pathway.Methods SD rats were divided randomly into five groups:control,DKD model,Xuezhikang(DKD modeling+1 200 mg/(kg·d)Xuezhikang by gavage),inhibitor group(DKD modeling+0.2 mg/(kg·d)AMPK inhibitor Compound C by intraperitoneal injection),and Xuezhikang+inhibitor(DKD modeling+1 200 mg/(kg·d)Xuezhikang by gavage+0.2 mg/(kg·d)AMPK inhibitor Compound C by intraperitoneal injection).Renal pathological changes,renal function indicators(24-hour urine albumin,serum creatinine(Scr),blood urea nitrogen(BUN)),expression levels of phosphorylated AMPK(p-AMPK)and eNOS,and levels of inflammatory indicators(tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)),oxidative stress indicators(superoxide dismutase(SOD)and malondialdehyde(MDA))in the kidneys were detected after 4 weeks of the respective interventions.Results Compared with the model group,renal pathological changes were alleviated,levels of 24-hour urinary albumin,Scr,BUN,TNF-α,IL-6,and MDA in the kidneys decreased,while expression levels of p-AMPK,eNOS,and SOD increased in the Xuezhikang group(P<0.05).In addition,renal pathological changes were aggravated,levels of 24-hour urinary albumin,Scr,BUN,TNF-α,IL-6,and MDA in the kidneys increased,while expression levels of p-AMPK,eNOS,and SOD decreased in the inhibitor group(P<0.05).Compared with the Xuezhikang group,renal pathological changes were aggravated,levels of 24-hour urinary albumin,Scr,BUN,TNF-α,IL-6,and MDA in the kidneys increased,while expression levels of p-AMPK,eNOS,and SOD decreased in the Xuezhikang+inhibitor group(P<0.05).Conclusions Xuezhikang alleviates renal injury and the inflammatory and oxidative stress responses in DKD rats by activating AMPK/eNOS.
韩小丽;赵琦;董娟;赵锦纹;蒋秀峰;卫志锋;刘翠兰
河北北方学院附属第一医院肾内科,河北 张家口 075000河北北方学院附属第一医院肾内科,河北 张家口 075000河北北方学院附属第一医院肾内科,河北 张家口 075000河北北方学院附属第一医院血液净化科,河北 张家口 075000河北北方学院附属第一医院肾内科,河北 张家口 075000河北北方学院附属第一医院肾内科,河北 张家口 075000河北北方学院附属第一医院肾内科,河北 张家口 075000
医药卫生
糖尿病肾病血脂康腺苷酸蛋白活化激酶内皮型一氧化氮合酶
diabetic kidney diseaseXuezhikangadenosine 5'-monophosphate-activated protein kinaseendothelial nitric oxide synthase
《中国比较医学杂志》 2026 (9)
55-62,8
张家口市科学技术局2024年市级科技计划(2421067D).
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