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 cells to 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-α-induced A549 cells. And their related transcription 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 cells to 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-α-induced A549 cells. And their related transcription 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.
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Keywords:
A549 cells; Chinese medical formula; Cigarette smoking; Tumor necrosis factor-alpha