RESUMEN

BACKGROUND: The traditional Chinese medicine NiuBeiXiaoHe (NBXH) extract and Chinese medicine preparation JieHeWan (JHW) exhibit anti-tuberculosis effects. The anti- tuberculosis effect of NBXH was compared with that of JHW to elucidate the mechanism of action of NBXH. METHODS: BALB/c mice aged 6-8 weeks were randomly divided into a normal control group, Tuberculosis (TB) model group, JHW treatment group, and NBXH treatment group. After 3 and 13 weeks of treatment, the therapeutic effect in each group was evaluated by comparing lung histopathology, lung and liver colony counts, the number of spots representing effector T cells secreting IFN-γ in an ELISPOT, and the levels of Th1, Th2, and Th17 cytokines, which were measured by a cytometric bead array (CBA). Mouse RNA samples were subjected to transcriptome sequencing. RESULTS: After 13 weeks of treatment, the mean histopathological lesion area of the NBXH group was significantly smaller than that of the TB model group (P < 0.05). Compared with those in the TB model group, the lung colony counts in the JHW and NBXH groups were significantly decreased (P < 0.05), and the IL-2 and IL-4 levels in the NBXH group were significantly increased (P < 0.05). NBXH partly restored significant changes in gene expression caused by Mycobacterium tuberculosis (M. tuberculosis) infection. According to GO and KEGG analyses, the changes in biological process (BP), cell composition (CC) and molecular function (MF) terms and in signaling pathways caused by NBXH and JHW treatment were not completely consistent, but they were mainly related to the immune response and inflammatory response in the mouse TB model. CONCLUSIONS: NBXH had therapeutic effects similar to those of JHW in improving lung histopathology, reducing lung colony counts, and regulating the levels of cytokines. NBXH restored significant changes in gene expression and repaired cell damage caused by M. tuberculosis infection by regulating immune-related pathways, which clarified the mechanism of action of NBXH.

Asunto(s)

Antituberculosos/farmacocinética , Medicamentos Herbarios Chinos/farmacocinética , Medicina Tradicional China/normas , Animales , Modelos Animales de Enfermedad , Medicamentos Herbarios Chinos/normas , Femenino , Pulmón/efectos de los fármacos , Pulmón/fisiología , Medicina Tradicional China/estadística & datos numéricos , Ratones , Ratones Endogámicos BALB C , Tuberculosis/tratamiento farmacológico

RESUMEN

OBJECTIVE To investigate the protective effect of Codonopsis Pilosula Polysaccharide (CPPS) on improving of the memory consolidation disorder induced by Cycloheximide and its possible mechanisms in mice. METHODS The mice was divided into five groups, as normal control group, cycloheximid model group, piracetam positive control group, CPPS 300 mg · kg- 1 group, and CPPS 150 mg·kg-1 group. The mice respectively were given saline, piracetam, and CPPS for 15 d. The memory consolidation disorder model in mice was established by ip. Cyclohexylamine, and orally administered CPPS(300 mg·kg-1 or 150 mg·kg-1) every day. Then experimental groups were subjected Morris Water Maze test. Western blotting analysis were used to analysis the expression of CaMKⅡ/CREB signaling pathways. RESULTS Morris water maze experiment showed that cyclohexylamine can cause memory consolidation disorder(P<0.01), and giving piracetam and CPPS (300 mg · kg- 1) can improve spatial memory impairment in mice(P<0.05, P<0.01). Western blotting experiment results show that compared with normal control group, CaMKⅡ and CREB contents of brain in model group mice had significant decreased(P<0.001); Compared with model group, CaMK Ⅱ and CREB contents of brain tissue in piracetam and CPPS groups increased significantly(P<0.05,P<0.01,P<0.001). CONCLUSION Cyclo?heximide can induce the memory consolidation disorder, and its effect in mice related to CaMK/CREB signaling pathways. CPPS can improved this memory disorder by influence CaMKⅡ/CREB signaling pathways.