前列腺炎I号通过MAPK信号通路缓解大鼠慢性非细菌性前列腺炎的抗炎机制研究

Study on Anti-Inflammatory Mechanism of Prostatitis I Formula(前列腺炎 I 号) Relieving Chronic Non Bacterial Prostatitis in Rats through MAPK Signal Pathway

目的探究前列腺炎I号在治疗大鼠慢性非细菌性前列腺炎的作用机制。方法 40只体质量180~200 g的8周龄的SD雄性大鼠,随机分为对照组、模型组、前列腺炎I号高低给药组,每组10只。剥取前列腺组织采用比浊法测定其蛋白浓度,临用前用0.01 mmol/L PBS调节至15 mg/mL。大鼠乙醚麻醉后,腹腔注射百白破疫苗0.5 mL,皮下多点注射前列腺蛋白提纯稀释液与FCA混合乳剂(1∶1体积)1 mL。30 d后,重复1次,即可诱导产生大鼠慢性非细菌性前列腺炎症。造模的同时按剂量高低组分别灌胃1000、500 m/kg的前列腺炎I号给药30 d。造模结束后经眼眶取血收集大鼠血浆,解剖取大鼠前列腺组织备用。结果在前列腺炎模型大鼠前列腺组织及血浆中转化生长因子β1(TGF-β1)的蛋白水平显著高于对照组,而前列腺炎I号有助于降低大鼠前列腺组织及血浆中TGF-β1的水平。组间比较模型组大鼠白介素-2(IL-2)及白介素-6(IL-6)显著升高,高低剂量前列腺炎I号治疗给药组大鼠炎症因子的水平较模型组显著下降,同时高剂量治疗组效果优于低剂量组。与对照组相比,在前列腺炎模型组大鼠的前列腺组织中存在着ERK1/2、JNK及P38蛋白的磷酸化水平的增多,但是ERK1/2、JNK及P38的总蛋白水平没有显著的变化,同时,前列腺炎I号高低剂量治疗组大鼠前列腺组织中ERK1/2、JNK及P38蛋白的磷酸化水平显著下降。结论前列腺炎I号能够通过抑制MAPK信号通路的过度激活而降低IL-2及IL-6炎症因子的表达,进而缓解大鼠前列腺炎。

Objective To explore the mechanism of Prostatitis I Formula(前列腺炎I号)in the treatment of chronic nonbacterial prostatitis in rats. Methods Forty SD male rats with a weight of 180-200 g of 8 weeks were randomly divided into control group, model group, Prostatitis I Formula high and low dose groups, each group with 10 rats. The protein concentration of prostate tissue was measured by turbidimetric method. Before use, 0.01 mmol/L PBS was adjusted to 15 mg/mL. After anesthesia with ether, rats were given 0.5 mL of budesophagosis vaccine, and the purified diluent of prostate protein and FCA mixed emulsion(1:1 volume) were injected subcutaneously for 1 mL. After 30 days, the operation was repeated once. The rats were induced to develop chronic non bacterial prostatitis. At the same time, the rats were given Prostatitis I Formula of 1000 m/kg and 500 m/kg respectively for 30 days according to the dose level group. After the model was completed, the rat plasma was collected by orbital blood collection, and the prostate tissue of rats was dissected for standby. Results The protein levels of TGF-β1 in the prostate tissue and plasma of the prostatitis model rats were significantly higher than that of the control group, and Prostatitis I Formula helped to reduce the levels of TGF-β1 in the rat prostate tissue and plasma. The expressions of inflammatory factors IL-2 and IL-6 in the prostate tissue and plasma of the model group were significantly higher than those of the control group, and the levels of inflammatory factors in the Prostatitis I Formula high and low dose groups were significantly lower than those of the model group. The effect of the Prostatitis I Formula high dose group was better than that of the low dose group. Compared with the control group, there was an increase in the phosphorylation levels of ERK1/2, JNK, and P38 proteins in the prostate tissue of the prostatitis model group, but there was no significant change in the total protein levels of ERK/2, JNK or P38. At the same time, the phosphorylation levels of ERK1/2, JNK and P38 protein in the prostate tissue of rats in the Prostatitis I Formula high and low dose groups were significantly decreased. Conclusion Prostatitis I Formula can reduce the expressions of IL-2 and IL-6 inflammatory factors by inhibiting the excessive activation of MAPK signaling pathway, thereby alleviating prostatitis in rats.