MCP-1/COX-2/P53在高脂饲料诱导的前列腺增生组织中的表达

Expression of MCP-1/COX-2/P53 in benign prostatic hyperplasia induced by high fat diet

目的通过高脂饲料大鼠模型,探讨炎症和凋亡因子在高脂饲料相关前列腺增生中的表达情况。方法将20只SD大鼠分为2组:对照组和高脂饲料组。42周时,测量各组大鼠的体长、腰围、体重以及腹股沟脂肪质量、附睾脂肪质量和前列腺质量,计算体重指数和前列腺指数,并通过ELISA和Western blotting检测各组大鼠的血清及前列腺组织参数。结果高脂饲料组大鼠的体重、腰围、体重指数、腹股沟脂肪质量、附睾脂肪质量、前列腺质量和前列腺指数均明显高于对照组(P<0.05)。高脂饲料组血清三酰甘油、低密度脂蛋白和胆固醇较对照组均明显升高(P<0.05),前列腺组织的肿瘤坏死因子α和单核细胞趋化蛋白-1 (MCP-1)表达均明显高于对照组(P<0.05)。Western blotting结果显示高脂饲料组大鼠前列腺的环氧化酶-2 (COX-2)表达明显高于对照组,而p53明显低于对照组。结论高脂饲料通过诱导慢性炎症导致前列腺生长和前列腺增生进展,而MCP-1和COX-2表达增加引起的炎症反应以及p53下调在上述过程中起关键作用。

Objective To investigate the expression of inflammatory and apoptotic factors in benign prostatic hyperplasia(BPH) induced by high fat diet(HFD) in rats. Methods Twenty SD rats were divided into two groups: a control group and HFD group. At 42 weeks, their body length, waist circumference, body weight,inguinal fat, epididymal fat and prostate weight were measured, body mass index(BMI) and prostate index calculated, and serum and prostate tissue parameters detected by ELISA and Western blotting. Results The body weight, waist circumference, body mass index, inguinal fat weight, epididymal fat weight, prostate weight and prostate index of rats in the HFD group were significantly higher than those in the control group(P< 0.05). The serum triglyceride, low density lipoprotein and cholesterol in the HFD group were significantly higher than those in the control group(P< 0.05);the expression of tumor necrosis factor α and monocyte chemotactic protein-1(MCP-1) in prostate tissue in the HFD group were significantly higher than those in the control group(P< 0.05). The results of Western blotting showed that the expression of cyclooxygenase-2(COX-2) was significantly higher and the expression of p53 was significantly lower in the HFD group than those in the control group. Conclusion HFD can induce the growth of prostate and the progression of BPH by inducing chronic inflammation, and the inflammatory response caused by the increased expression of MCP-1 and COX-2 and the down-regulation of p53 plays a key role in the process.