2015年全球结核新增病例大约为1040万例、死于结核的约为140万人。结核短程治疗方案需要服药6个月，因部分病人不能坚持服药，导致复发并容易出现耐药菌。因此，缩短结核治疗时间是控制结核的关键措施。结核杆菌在病灶形成生物膜，保护菌体免受药物和免疫攻击，是结核治疗时间长的原因。为此，我们提出“生物膜抑制剂与抗痨药物联合用药缩短结核治疗时间”的假说。使用生物膜抑制剂破坏生物膜结构，暴露生物膜内的结核杆菌，再由抗痨药物杀死结核杆菌。前期工作表明，瑶山南星乙醇提取物能抑制并破坏结核杆菌生物膜，异烟肼、 利福平与瑶山南星组合均能有效杀死生物膜内的结核杆菌。为了证实这一假说，我们拟从瑶山南星跟踪分离生物膜抑制剂，探索其作用机制，最后采用康奈尔小鼠模型验证生物膜抑制剂与抗痨药物联合用药的药效。本课题将为探索结核杆菌的致病性提供新的分子探针，为治疗结核提供新的思路，研究成果具有重要的理论意义和应用前景。

The most recent World Health Organization (WHO) estimates of the global burden of TB are staggering: in 2015, there were 10.4 million prevalent cases of active TB, with 1.4 million deaths attributable to this disease. The current short-course regimen for human tuberculosis consists of the daily administration of multiple drugs for 6 months. However, some patients can not adhere to this drug regimen, which are the cause of relapse and prone to emergence of drug resistance. Therefore, shortening the treatment time of tuberculosis is the key measure to control the tuberculosis. Mycobacterium tuberculosis could form biofilm in the focus during infection, which protect the bacillus from drugs and immune attacks. It is the main reason for the long time of treatment of tuberculosis. So we propose that the combination of biofilm inhibitor and antituberculosis agents might shorten the time of treatment of tuberculosis. If the biofilm were disrupted by biofilm inhibitor, Mycobacterium tuberculosis that entrapped within the biofilm will be exposed to the antituberculosis agents and be killed. Our preliminary work showed that the ethanol extract of Arisaema sinii whole plants could inhibit and disrupt Mycobacterium tuberculosis biofilm. Experiments in vitro also indicated that the combination of Isoniazid or rifampicin and the ethanol extract of A. sinii showed powerful activities to kill Mycobacterium tuberculosis within the biofilm. In order to verify above hypothesis, we will establish the bioassay-guided isolation method to isolate the biofilm inhibitor from the extract of A. sinii whole plants, and to investigate the inhibiting mechanism, and finally to verify the efficacy of the new strategy to fight against tuberculosis based on Cornell mouse model. This study will provide a new molecular probe to explore the pathogenicity of Mycobacterium tuberculosis in animal, and suggest a new way to control tuberculosis. Therefore, this study will produce an important theoretical significance on tuberculosis treatment and have a potential application value.