Higuchi Y, Ono K, Sekita S, Onodera H, Mitsumori K, Nara Y, Satake M
Division of Pharmacognosy and Phytochemistry, National Institute of Health Sciences, Tokyo, Japan.
Biol Pharm Bull. 1998 Sep;21(9):914-8. doi: 10.1248/bpb.21.914.
Shichimotsu-koka-to (SKT) has been prescribed to treat patients with essential and renal hypertension. We investigated the effects of SKT on renal lesions in stroke-prone spontaneously hypertensive rats (SHRSPs). SHRSPs were given an extract of SKT by mixing it with drinking water, from 8 through 29 weeks of age, so that the average intake of SKT extract was about 1.5 g/kg/d. At 29 weeks of age, the kidneys of SHRSPs exhibited proliferative arteritis characterized by the proliferation of smooth muscle cells in the interlobular arteries, dilation and degeneration of renal tubules, infiltration of inflammatory cells and hemorrhage, with partial swelling or necrotizing of glomeruli. In particular, arteritis and periarteritis were noted. The treatment of SHRSPs with SKT ameliorated this morphological damage in the kidney and significantly decreased urea nitrogen in the serum. Treatment with SKT also strongly decreased the xanthine oxidase (XOD) activity and significantly increased the superoxide dismutase (SOD) activity in the kidney of SHRSPs; consequently, these values became close to those in normotensive Wistar Kyoto rats (WKYs). These results indicate that treatment with SKT ameliorated the histopathological damage and change in activity of enzymes related to free radicals in the kidney of SHRSPs, which may be important mechanisms for SKT for protecting SHRSPs from renal dysfunction.
六味地黄丸（SKT）已被用于治疗原发性高血压和肾性高血压患者。我们研究了SKT对易卒中型自发性高血压大鼠（SHRSPs）肾脏病变的影响。从8周龄到29周龄，将SKT提取物与饮用水混合后给予SHRSPs，使SKT提取物的平均摄入量约为1.5 g/kg/d。在29周龄时，SHRSPs的肾脏表现出增生性动脉炎，其特征为小叶间动脉平滑肌细胞增生、肾小管扩张和变性、炎症细胞浸润和出血，伴有部分肾小球肿胀或坏死。特别值得注意的是动脉炎和动脉周围炎。用SKT治疗SHRSPs可改善肾脏的这种形态学损伤，并显著降低血清尿素氮水平。用SKT治疗还可强烈降低SHRSPs肾脏中的黄嘌呤氧化酶（XOD）活性，并显著提高超氧化物歧化酶（SOD）活性；因此，这些值接近正常血压的Wistar Kyoto大鼠（WKYs）。这些结果表明，用SKT治疗可改善SHRSPs肾脏的组织病理学损伤和与自由基相关的酶活性变化，这可能是SKT保护SHRSPs免受肾功能障碍的重要机制。
