论文部分内容阅读
目的:观察生精胶囊对肾小球病肾病综合征大鼠转化生长因子β1(TGFβ)1、结缔组织生长因子(CTGF)、细胞外基质(ECM)的影响,探索中药制剂防护肾损害的可能机制。方法:将30只SD大鼠分为对照组、模型组、治疗组各10只。对照组不造模;模型组采用2次注射阿霉素(ADR)方法建立肾小球病肾病综合征的模型;治疗组造模同模型组,并于第1次注射ADR后每天1次中药制剂生精胶囊灌胃,各组均在4周后观察肾皮质部层黏连蛋白(LN)、纤维连接蛋白(FN)、Ⅳ型胶原(ColⅣ)蛋白的表达;并检测肾皮质部TGFβ1 mRNA、CTGF mRNA的表达。结果:造模后模型组、治疗组LN、FN(治疗组除外)、ColⅣ蛋白表达半定量升高,与对照组比较,差异均有非常显著性意义(P<0.01)。治疗后治疗组LN、FN、ColⅣ蛋白表达半定量均有不同程度降低,与模型组比较,差异有显著性或非常显著性意义(P<0.05,P<0.01)。造模后模型组、治疗组TGFβ1 mR NA、CTGF mR NA表达量升高,与对照组比较,差异均有非常显著性意义(P<0.01)。治疗后治疗组TGFβ1 mR-NA、CTGF mR NA表达量有不同程度降低,与模型组比较,差异有显著性或非常显著性意义(P<0.05,P<0.01)。结论:中药制剂生精胶囊可通过下调细胞因子TGFβ1和CTGF的表达来降低ECM合成,减少ECM的积聚,从而拮抗细胞因子对肾脏的损害作用。
Objective: To observe the effect of shenjing capsule on transforming growth factor β1 (TGFβ1), connective tissue growth factor (CTGF) and extracellular matrix (ECM) in rats with nephritic syndrome of glomerular nephropathy, and to explore the possible protective effect of traditional Chinese medicine on renal damage mechanism. Methods: 30 SD rats were divided into control group, model group and treatment group. The control group was not model. The model group was established with two injections of adriamycin (ADR) to establish the model of nephrotic syndrome of glomerular disease. The model group was established in the treatment group and once a day with the traditional Chinese medicine The spermatogenic capsules were intragastrically administrated. The expressions of LN, FN and ColⅣ in renal cortex were observed after 4 weeks. The expressions of TGFβ1 mRNA , CTGF mRNA expression. Results: After modeling, the expression of Col Ⅳ protein in model group and treatment group were increased semiquantitatively except for LN and FN (except for treatment group), and the difference was significant (P <0.01) compared with control group. After treatment, the semiquantitative expression of LN, FN and ColⅣ in the treatment group decreased to some extent. Compared with the model group, the difference was significant or very significant (P <0.05, P <0.01). After modeling, the expression of TGFβ1 mR NA and CTGF mR NA in model group and treatment group increased significantly compared with the control group (P <0.01). After treatment, the expression levels of TGFβ1 mR-NA and CTGF mR NA in the treatment group decreased to some extent. There was significant or very significant difference between the treatment group and the model group (P <0.05, P <0.01). CONCLUSION: SSP can inhibit the synthesis of ECM by decreasing the expression of cytokines TGFβ1 and CTGF, reduce the accumulation of ECM, and thus antagonize the cytotoxic effects of cytokines on the kidneys.