薯蓣皂苷对脓毒症大鼠肾损伤的影响及机制
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篇名: 薯蓣皂苷对脓毒症大鼠肾损伤的影响及机制
TITLE: Effect and mechanism of dioscin on renal injury in septic rats
摘要: 目的 探究薯蓣皂苷对脓毒症大鼠肾损伤的影响及可能机制。方法采用盲肠结扎和穿刺法建立脓毒症大鼠模型。将建模成功的60只大鼠按照随机数字表法分为模型组(0.5%羧甲基纤维素钠溶液),薯蓣皂苷低、中、高剂量组(30、60、120mg/kg)和地塞米松组(阳性对照,10mg/kg),每组12只;另取12只大鼠作为假手术组(0.5%羧甲基纤维素钠溶液)。造模15min后,各组大鼠尾静脉注射给药/0.5%羧甲基纤维素钠溶液。给药24h后,检测大鼠血清中肌酐(Cr)、尿素氮(BUN)、中性粒细胞明胶酶相关脂质运载蛋白(NGAL)、肾损伤分子1(KIM-1)、白细胞介素6(IL-6)、IL-1β、肿瘤坏死因子α(TNF-α)水平以及肾组织中丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性和核因子E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)、NOD样受体蛋白3(NLRP3)表达量,并观察肾组织病理形态学变化。结果与模型组比较,薯蓣皂苷低、中、高剂量组大鼠肾组织病理损伤明显改善,血清中Cr、BUN、NGAL、KIM-1、IL-6、IL-1β、TNF-α水平和肾组织中MDA水平、NLRP3蛋白表达量均显著降低(P<0.05),肾组织中SOD活性和Nrf2、HO-1蛋白表达量均显著升高(P<0.05),且薯蓣皂苷的作用具有剂量依赖性(P<0.05);薯蓣皂苷高剂量组和地塞米松组大鼠肾组织病理损伤情况相似,上述指标水平差异均无统计学意义(P>0.05)。结论薯蓣皂苷可能是通过激活Nrf2/HO-1信号通路抑制NLRP3炎性小体,实现对炎症因子表达和氧化应激的抑制,从而发挥对脓毒症肾损伤的保护作用。
ABSTRACT: OBJECTIVE To investigate the effect of dioscin on renal injury in septic rats and its possible mechanism. METHODS The septic rat model was induced by using cecal ligation and puncture. Sixty model rats were randomly divided into model group (0.5% sodium carboxymethyl cellulose solution), dioscin low-dose, medium-dose and high-dose groups (30, 60, 120 mg/kg) and dexamethasone group (positive control, 10 mg/kg), with 12 rats per group; another 12 rats were selected as the sham operation group (0.5% sodium carboxymethyl cellulose solution). After 15 minutes of modeling, rats in each group were injected with medicine/0.5% sodium carboxymethyl cellulose solution via the tail vein. Twenty-four hours after administration, the levels of creatinine (Cr), blood urea nitrogen (BUN), neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule-1 (KIM- 1), interleukin 6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α) in serum and malondialdehyde (MDA) in renal tissue, superoxide dismutase (SOD) activity and the protein expressions of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NOD-like receptor protein 3 (NLRP3) were detected; renal histomorphology was observed. RESULTS Compared with model group, pathological injury of renal tissue was improved significantly in dioscin low-dose, medium-dose and high-dose groups; the levels of Cr, BUN, NGAL, KIM-1, IL-6, IL-1β and TNF-α in serum, MDA level and protein expression of NLRP3 in renal tissue were decreased significantly (P<0.05); SOD activity in renal tissue, protein expressions of Nrf2 and HO-1 were increased significantly (P<0.05), in a dose-dependent manner (P<0.05). The pathological damage of renal tissue in the dioscin high-dose group was similar to dexamethasone group, and there was no statistically significant difference in the levels of the above indicators (P>0.05). CONCLUSIONS Dioscin can activate the Nrf2/HO-1 signaling pathway to inhibit NLRP3 inflammasome, and realize the inhibition of inflammatory factors and oxidative stress, so as to protect the kidney injury in sepsis.
期刊: 2024年第35卷第11期
作者: 申翔;徐尚刚;黄洋辉;罗斌;周裕丰;梁隆斌
AUTHORS: SHEN Xiang,XU Shanggang,HUANG Yanghui,LUO Bin,ZHOU Yufeng,LIANG Longbin
关键字: 薯蓣皂苷;Nrf2/HO-1信号通路;NLRP3炎性小体;脓毒症;肾损伤
KEYWORDS: dioscin; Nrf2/HO-1 signaling pathway; NOD-like receptor protein 3 inflammasome; sepsis; renal injury
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