目的探讨葡萄籽原花青素(grape seed proanthocyanidins,GSP)对氯化镉染毒大鼠肾细胞DNA损伤的拮抗作用。方法将32只健康雄性SPF级SD大鼠按体重随机分为4组,分别为对照组(腹腔注射、灌胃生理盐水)、镉染毒组(腹腔注射1.5 mg/kg氯化镉溶液和灌胃生理盐水)和低、高剂量GSP干预组(腹腔注射1.5 mg/kg氯化镉,同时,分别灌胃20、40 mg/kg GSP溶液),每组8只。腹腔注射和灌胃染毒容量分别为3、5 ml/kg,连续染毒14 d。采用单细胞凝胶电泳技术(SCGE)检测肾细胞的DNA损伤,采用实时荧光RT-PCR技术检测c-jun N末端激酶(JNK)、p38丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)mRNA的表达。结果与对照组比较,镉染毒组大鼠肾脏细胞DNA的尾长、Olive尾矩、尾矩均显著升高,差异具有统计学意义(P<0.05)。低、高剂量GSP干预组大鼠肾脏细胞的DNA损伤均高于对照组,但差异无统计学意义。各剂量GSP干预组大鼠肾脏细胞DNA的尾长、Olive尾矩、尾矩均显著低于镉染毒组差异有统计学意义(P之0.05)。且随着GSP染毒剂量的升高,镉染毒大鼠肾脏细胞的尾长、Olive尾矩、尾矩均呈下降趋势。与镉染毒组比较,各剂量GSP干预组大鼠肾脏细胞中JNK mRNA的表达水平均显著下降,差异有统计学意义(P<0.05);而p38 MAPK mRNA的表达水平无显著变化。结论 GSP可能通过降低MAPK信号通路中JNK的表达拮抗氯化镉诱发的大鼠肾细胞DNA损伤效应。 Objective To investigate the antagonistic effect of grape seed proanthocyanidins (GSP) on DNA damage induced by cadmium chloride in rat kidney cells. Methods Thirty-two male Sprague-Dawley (SD) SD rats were randomly divided into four groups according to body weight: control group (intraperitoneal injection, normal saline), cadmium exposure group (intraperitoneal injection of 1.5 mg / kg cadmium chloride solution and irrigation Gastric saline) and low and high dose GSP intervention groups (intraperitoneal injection of 1.5 mg / kg cadmium chloride, respectively, at the same time, respectively, gavage 20,40 mg / kg GSP solution), each group of eight. Intraperitoneal injection and intragastric administration capacity were 3,5 ml / kg, continuous exposure to 14 d. Single cell gel electrophoresis (SCGE) was used to detect DNA damage in renal cells. Real-time fluorescent RT-PCR was used to detect the expression of c-jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase ) mRNA expression. Results Compared with the control group, the tail length, Olive tail moment and tail moment of DNA in the kidney of cadmium-exposed rats were significantly increased, with statistical significance (P <0.05). The DNA damage of kidney cells in low and high dose GSP intervention groups was higher than that in control group, but the difference was not statistically significant. The tail length, Olive tail moment and tail moment of rat kidney cells in each dose of GSP intervention group were significantly lower than those in cadmium exposure group (P <0.05). And with the increase of GSP dose, tail length, Olive tail moment and tail moment of cadmium-exposed rats decreased. Compared with cadmium exposure group, the expression of JNK mRNA in renal cell of GSP group was significantly decreased (P <0.05), while the expression level of p38 MAPK mRNA had no significant change. Conclusion GSP may antagonize cadmium chloride-induced DNA damage induced by cadmium chloride in rats by decreasing the expression of JNK in MAPK signaling pathway.