枸杞多糖对糖尿病肾损伤的保护作用和机制研究

目的：研究枸杞多糖（Lycium barbarum polysaccharide, LBP）对大鼠糖尿病肾损伤的保护作用及机制。方法：腹腔注射链脲佐菌素（streptozotocin, STZ）建立大鼠糖尿病（diabetes mellitus, DM）模型。将大鼠分为对照组、糖尿病组、LBP（60 mg/kg）组和LBP（30 mg/kg）组。LBP组灌胃给予LBP,每天一次,持续12周。测定大鼠空腹血糖值、血肌酐（serum creatinine, Scr）、血尿素氮（blood urea nitrogen, BUN）、C反应蛋白（C-reactive protein, CRP）、肿瘤坏死因子（tumor necrosis factor-α, TNF-α）、白细胞介素-6（ interleukin-6, IL-6）的含量。计算相对肾质量,观察肾脏组织形态变化,测定肾组织中超氧化物歧化酶（superoxide dismutase, SOD）、过氧化氢酶（catalase, CAT）、谷胱甘肽过氧化物酶（glutathione peroxidase, GSH-Px）活性、谷胱甘肽（glutathione, GSH）、丙二醛（malondialdehyde, MDA）的含量,核转录因子-кB（nuclear factor-kappa B, NF-кB）亚基p65、细胞间黏附分子-1（intercellular adhesion molecule-1, ICAM-1）和单核细胞趋化蛋白-1（monocyte chemotactic protein-1, MCP-1）表达。结果：与对照组相比,糖尿病组大鼠血糖明显升高（≥16.7 mmol/L）,血清中Scr、BUN、CRP、IL-6、TNF-α含量增加,肾组织MDA含量提高,GSH含量和GSH-Px、CAT、SOD活性降低,NF-кB亚基p65、MCP-1和ICAM-1表达水平增加。而与糖尿病组相比,LBP能降低糖尿病大鼠的血糖,减少血清中Scr、BUN、CRP、IL-6、TNF-α的含量,降低肾组织MDA含量,提高GSH含量、GSH-Px、CAT、SOD活性,下调NF-кB亚基p65、MCP-1和ICAM-1表达水平。 结论：LBP对糖尿病肾损伤具有明显的保护作用,其作用机制可能与其改善糖尿病大鼠血糖,降低肾脏氧化应激水平和减轻炎症反应有关。

Protective effect and mechanism of lycium barbarum polysaccharides on diabetic renal injury

AIM: To study the protective effect and mechanism of Lycium barbarum polysaccharide (LBP) on diabetic kidney injury in rats. METHODS: Intraperitoneal injection of streptozotocin (STZ) to establish a rat model of diabetes (DM). The rats were divided into control group, diabetes group, LBP (60 mg/kg) group and LBP (30 mg/kg) group. The LBP group was given LBP by gavage once a day for 12 weeks. Determination of rat fasting blood glucose level, blood creatinine (Scr), urea nitrogen (BUN), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) content. Calculate relative kidney mass, observe changes in kidney tissue morphology, and determine superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activity, and glutathione (GSH) in kidney tissue, malondialdehyde (MDA) content, nuclear factor-кB (NF-кB) subunit p65, intercellular adhesion molecule-1 (ICAM-1) andmonocyte chemotactic protein-1 (MCP-1) expression. RESULTS: Compared with the control group, the blood glucose of rats in the diabetic group was significantly increased (≥16.7 mmol/L), the content of Scr, BUN, CRP, IL-6, and TNF-α in the serum increased, the content of MDA in the kidney tissue increased, and the content of GSH increased And GSH-Px, CAT, SOD activity decreased, NF-кB subunit p65, MCP-1 and ICAM-1 expression levels increased. Compared with the diabetes group, LBP can reduce blood glucose in diabetic rats, reduce the serum levels of Scr, BUN, CRP, IL-6, and TNF-α, reduce the content of MDA in kidney tissue, increase the content of GSH, GSH-Px, CAT, SOD, and down-regulate the expression levels of NF-кB subunit p65, MCP-1 and ICAM-1. CONCLUSION: LBP has a significant protective effect on diabetic kidney injury, and its mechanism of action may be related to the improvement of blood glucose, reduction of renal oxidative stress and reduction of inflammatory reaction in diabetic rats.