摘要
OBJECTIVE: To investigate the efficacy of Tiaobu Feishen formulae(TBFS), including Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF), on inflammatory response, protease-anti-protease imbalance and collagen deposition in rats.METHODS: In present work, we used an in vitro model of cigarette smoking extract(CSE)-and tumor necrosis factor-α(TNF-α)-induced A549 cellsto examine the efficacy of BJF, BYF and YZF on the production of inflammatory cytokines, including TNF-α and interleukin(IL)-8, IL-6, matrix metalloproteinases(MMP)-9, and IL-10 in CSE or TNF-ls. And their related transcripα-induced A549 celtion factors and signaling pathway were also analyzed.RESULTS: The results showed that BJF, BYF and YZF could significantly decrease the expression levels of the pro-inflammatory cytokines induced by CSE or TNF-α. Furthermore, BJF, BYF and YZF could suppress CSE-or TNF-α-induced activation of nuclear factor-kappa B(NF-κB) transcription factors and its corresponding pathways. Taken together, these data implied that BJF, BYF and YZF effectively inhibited CSE-or TNF-α-induced inflammatory response in alveolar epithelial cell, which was due to their inhibition effect on NF-κB pathways.CONCLUSION: Our findings suggest that the Tiaobu Feishen therapies may protect human alveolar epithelial cells against cigarette smoking and TNF-α-induced inflammation. NF-κB pathway may involve in the actions.
OBJECTIVE: To investigate the efficacy of Tiaobu Feishen formulae(TBFS), including Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF), on inflammatory response, protease-anti-protease imbalance and collagen deposition in rats.METHODS: In present work, we used an in vitro model of cigarette smoking extract(CSE)-and tumor necrosis factor-α(TNF-α)-induced A549 cellsto examine the efficacy of BJF, BYF and YZF on the production of inflammatory cytokines, including TNF-α and interleukin(IL)-8, IL-6, matrix metalloproteinases(MMP)-9, and IL-10 in CSE or TNF-ls. And their related transcripα-induced A549 celtion factors and signaling pathway were also analyzed.RESULTS: The results showed that BJF, BYF and YZF could significantly decrease the expression levels of the pro-inflammatory cytokines induced by CSE or TNF-α. Furthermore, BJF, BYF and YZF could suppress CSE-or TNF-α-induced activation of nuclear factor-kappa B(NF-κB) transcription factors and its corresponding pathways. Taken together, these data implied that BJF, BYF and YZF effectively inhibited CSE-or TNF-α-induced inflammatory response in alveolar epithelial cell, which was due to their inhibition effect on NF-κB pathways.CONCLUSION: Our findings suggest that the Tiaobu Feishen therapies may protect human alveolar epithelial cells against cigarette smoking and TNF-α-induced inflammation. NF-κB pathway may involve in the actions.
基金
National Natural Science Fund of China(No.81130062,No.81403367)
Outstanding Traditional Chinese Medicine Academic Leader Program of Henan Province(No.HNZYLJ201301001)
the National Key Technology R&D Program during the 12th Five-Year Plan Period(No.2014BAI10B06)
