中文摘要：

目的初步探讨KCTD9在暴发性肝炎模型小鼠中的作用机制。方法78只BALB／cJ小鼠（其中雄性6只）随机分为暴发性肝炎对照组和暴发性肝炎模型组，每组39只（每组雄性3只）；75只C3H／HeJ雌性小鼠分为慢性肝炎对照组（36只）和慢性肝炎模型组（39只）。模型组每只小鼠腹腔注射MHV-3（100PFU）。暴发性肝炎对照组和模型组48h试验点以1只雄性小鼠供取睾丸，2只雌性小鼠供取肝脾等组织标本和分离肝细胞，10只雌性小鼠为1个单位取肝组织供分离肝脾淋巴细胞；慢性肝炎对照组和模型组48h时以1只小鼠供取肝脾组织，1只小鼠供分离肝细胞，10只为1个单位供分离肝脾淋巴细胞，重复3次，剩下3只小鼠在建模15d时处死，仅供取肝脾组织。磁珠分选肝脾单个核细胞，采用免疫组织化学、实时定量PCR技术检测KCTD9在暴发性肝炎、慢性肝炎模型动物中的表达差异，各组间比较用f检验或方差分析。结果与对照组比较，KCTD9mRNA在暴发性肝炎模型组小鼠肝CD8＋T细胞、CD4＋T细胞、自然杀伤细胞（NK）细胞中分别上调8．8倍、59．4倍、577．1倍，f值分别为-5．393、-3．706和-4．714，P值均〈0．05，差异有统计学意义；在脾CD4＋T细胞、CD8＋T细胞中，KCTD9mRNA表达水平分别下调了43％和69％，t值分别为2．906、10．98，P值均〈0．05，差异有统计学意义。与对照组比较，在慢性肝炎模型组小鼠肝NK细胞和CD4＋T细胞中KCTD9mRNA分别下调71％、51％，t值分别为3．827、5．746，P值均〈0．05，差异有统计学意义。KCTD9蛋白在暴发性肝炎模型组小鼠肝细胞中呈弱阳性表达，坏死灶周围及组织中炎症浸润细胞中呈强阳性表达；脾中阳性细胞仍散在分布，与对照组比较，脾白髓中细胞数量减少达71％。结论KCTD9在MHV-3诱导的暴发眭肝炎模型小鼠肝脏高表达，可能参与疾病发生和发展过程。

英文摘要：

Objective To explore the mechanisms of a novel potassium channel gene named KCTD9 （potassium channel tetramerisation domain containing 9） in model of fulminant viral hepatitis induced by murine hepatitis virus 3 （MHV-3）. Methods 78 BALB/cJ mice（6 male） were randomly and equally assigned to two groups, model group of fulminant viral hepatitis induced by MHV3 and its control. 75 C3H/HeJfemale mice were done into two groups, 39 for model group of chronic hepatitis induced by MHV3, 36 for control. Various samples including spleen, liver and lymphocytes from mice of two model groups and the controls were examined for KCTD9 expression by real time quantitative PCR and Immunohistochemistry. Independent-sanlples T test or one-way ANOVA were carried out in different groups. Results Increased expressions of KCTD9 mRNA was observed in livers of both model mice of fulminant viral hepatitis and chronic hepatitis. Compared with the control mice, the expressions of KCTD9 mRNA were up-regulated by 577.1-, 8.8-, 59.4- and 10.8-fold in hepatic NK cells, CD4＋ T cells, CDS＋ T cells and splenic NK cells respectively in model mice of fulminant viral hepatitis 48hr post MHV-3 infection, whereas down-regulation by 43% and 69% in splenic CD4 ＋ T cells and CD8＋ T cells were found respectively. In contrast, in model mice of chronic viral hepatitis the expressions of KCTD9 mRNA were down-regulated by71% and 51% in hepatic CD4＋ T cells and NK cells, respectively. The expression of KCTD9 protein was mainly evidenced in infiltrative monouclear cells of liver as shown by immunohistochemistry. Basal expression was also investigated and showed constitutive expression of KCTD9 in brain, thymus and other organs in BALB/cJ mice. Conclusion A novel potassium channel gene KCTD9 was highly expressed in hepatic NK cells and T cells of fulminant hepatitis mice induced by MHV-3.