摘要目的 探讨灵芝酸治疗大鼠原发性高血压的作用及机制.方法 雄性原发性高血压大鼠(SHR)30只,随机分成对照组、灵芝组、阳性组.各组SHR在常规喂养的基础上,对照组给以蒸馏水10 ml/kg,灵芝组给以灵芝酸0.6 g/kg,阳性组给以卡托普利0.03 g/kg,1次/d,灌胃.8周后,采血5 ml检测相关生化指标,同时解剖各组SHR,取主动脉作检测样本,用反转录聚合酶链式反应(RT-PCR)技术,检测超氧化物歧化酶(SOD)、一氧化氮合成酶(NOS)及高密度脂蛋白(HDL)的基因表达,用流式细胞术检测内皮细胞的凋亡.结果 治疗8周后,灵芝组SHR的血压趋于正常,血压(112.6±3.2)mm Hg(P＜0.01)；灵芝组SHR的SOD、NOS、HDL的基因表达明显上调,内皮细胞的凋亡率显著下降(P＜0.01)；灵芝组SHR的一氧化氮(NO)的生成显著增加,内皮素-1(ET-1)、丙二醛(MDA)的含量均显著下降(P＜0,01).灵芝组SHR的低密度脂蛋白(LDL)显著降低,HDL显著升高(P＜0.01).结论 灵芝酸可通过促进SOD的基因表达,提高SOD活性,清除自由基；促进NOS的基因表达,增加NO的生成；抑制内皮细胞的凋亡,从而改善和恢复内皮细胞的功能,发挥有效的降压功能.

abstractsObjective To investigate the effect and mechanism of ganoderma acid in therapy of the rat essential hypertension.Methods 30 male spontaneously hypertensive rat (SHR) were divided randomly into three groups:control group (CG),ganoderma acid group (Gan) and captoril (Cap) as positive control group.SHR were fed with distilled water (10 ml/kg) in control group,ganoderma acid (0.6 g/kg ) in Gan group,catopril (0.03 g/kg) in Cap group.After 8-weeks therapy,5 ml blood was extracted,rats in every group were sacrificed to get the aorta.The mRNA expression of superoxide dismutase (SOD),nitric oxide synthase (NOS) and high density lipoprotein (HDL) were detected by RT-PCR and the apoptosis of endothelial cells were measured by flowcytometry.Results After the 8 weeks therapy,as compared with the CG group,blood pressure of SHR in Gan group became stable[(112.6±3.2) mm Hg](P＜0.01).The expression of SOD,NOS and HDL showed obviously upregulated,and apoptosis of endothelial cell decreased significantly (P＜0.01).NO contents increased,and MDA,ET-1 decreased (P＜0.01).The contents of LDL decreased and HDL increased (P＜0.01).Conclusions Ganoderma acid may improve the function of endothelial cell and decrease the blood pressure by promoting the mRNA expression and activity of SOD,cleaning the radical ions and inhibiting the apoptosis of the endothelial cell.