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Mechanisms underlying the activation of cytotoxic function mediated by hepatic lymphocytes following the administration of glycyrrhizin.

机译:甘草甜素给药后由肝淋巴细胞介导的细胞毒性功能激活的潜在机制。

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摘要

Stronger neo-minophagen C (SNMC), a glycyrrhizin (GL) preparation, has been used for the treatment of chronic viral hepatitis. It has been reported that a single administration of SNMC induced the activation of hepatic lymphocytes in number and function in animal studies. However, it is still unknown how SNMC augments the cytotoxic function and why such augmentation of cytotoxicity occurs in the liver and other organs. In this study, SNMC was daily injected into mice (2 mg GL/day/mouse) for 2 weeks. A significant augmentation of cytotoxicity mediated by NK cells, NKT cells and TNFalpha was demonstrated mainly in the liver. The presence of TNFalpha-mediated cytotoxicity in the liver was demonstrated for the first time. In contrast to CD8+ cytotoxic T cells (CD8+ CTL), all these cytotoxicities were preexistent in lymphocytes without the immunization of a specific antigen or alloantigens. NK cytotoxicity was mediated by a perforin system, while NKT cytotoxicity was mediated by a Fas ligand system. The present results suggest that the entire cytotoxic function mediated by hepatic lymphocytes was simultaneously augmented by SNMC.
机译:更强的新诺法辛C(SNMC),一种甘草甜素(GL)制剂,已用于治疗慢性病毒性肝炎。据报道,在动物研究中,单次施用SNMC可诱导肝淋巴细胞的活化。然而,仍不知道SNMC如何增强细胞毒性功能以及为什么这种增强的细胞毒性在肝脏和其他器官中发生。在这项研究中,每天向小鼠注射SNMC(2 mg GL /天/小鼠),持续2周。主要在肝脏中证实了由NK细胞,NKT细胞和TNFα介导的细胞毒性的显着增强。首次证明了TNFα介导的细胞毒性在肝脏中的存在。与CD8 +细胞毒性T细胞(CD8 + CTL)相比,所有这些细胞毒性在没有免疫特定抗原或同种抗原的情况下都存在于淋巴细胞中。 NK细胞毒性由穿孔素系统介导,而NKT细胞毒性由Fas配体系统介导。目前的结果表明,SNMC同时增强了由肝淋巴细胞介导的全部细胞毒性功能。

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