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现在,广为应用的肝脏药,其中大部分是以改善受损害的肝细胞代谢,促进肝细胞再生,从而达到改善肝脏病理的目的。近年来,随着肝炎病毒知识的进展,病毒性肝炎肝细胞损害的机制正在被阐明,认为肝炎的发病并非肝炎病毒的直接作用,而是宿主以肝炎病毒的某种抗原作为靶子的免疫反应,尤其是细胞性免疫。对于慢性肝炎、肝硬化等慢性肝疾患来说,肝炎病毒的持续感染是必要的条件。以排除这种持续感染为目的,干扰素、阿糖腺嘌呤(ara—A)等抗病毒剂被用于HBe抗原阳性,DNA多聚酶阳性的慢性活动性肝炎的治疗。另一方面,通过增强宿主的免疫反应,以排除肝炎病毒为目的,cianidanol、OK—432,肾上腺皮质激素等免疫抑制剂作为免疫调节方法而被试用。这些药物治疗不能完全切断乙型肝炎病毒(HBV)持续感染,而是仅促进从HBe抗原向HBe抗体的血清转换(seroconversion),就治疗效果来说是有限的。
Now, the widely used liver medicine, most of which is to improve the damage of liver cell metabolism, promote liver cell regeneration, so as to achieve the purpose of improving liver pathology. In recent years, with the progress of hepatitis virus knowledge, the mechanism of liver cell damage of viral hepatitis is being clarified. It is thought that the incidence of hepatitis is not the direct effect of hepatitis virus but an immune response targeted by some host antigen of hepatitis virus. Especially cellular immunity. For chronic hepatitis, cirrhosis and other chronic liver disease, hepatitis virus continuous infection is necessary conditions. To exclude this persistent infection, antiviral agents such as interferon and ara-A are used in the treatment of HBe antigen-positive and DNA polymerase-positive chronic active hepatitis. On the other hand, immunosuppressive agents such as cianidanol, OK-432, adrenocortical hormone and the like are tested as immunomodulatory methods by enhancing host immune responses and excluding hepatitis viruses. Rather than completely severing the hepatitis B virus (HBV) persistent infection, these drug treatments only promote seroconversion from the HBe antigen to the HBe antibody, with limited therapeutic effects.