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 i...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.展开更多
OBJECTIVE: To investigate the therapeutic efficacy of Tiaobu Feishen formulae(TBFS) on cigarette smoke-induced inflammation in vitro using lipopolysaccharide(LPS)-induced and cigarette smoke extract(CSE)-induced NCI-H...OBJECTIVE: To investigate the therapeutic efficacy of Tiaobu Feishen formulae(TBFS) on cigarette smoke-induced inflammation in vitro using lipopolysaccharide(LPS)-induced and cigarette smoke extract(CSE)-induced NCI-H292 cells.METHODS: We evaluated the inhibitory effects of Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF) on the expressions of inflammatory cytokines including tumor necrosis factor(TNF)-α and interleukin(IL)-8, matrix metalloproteinase(MMP)-9, tissue inhibitor of matrix metalloprotease(TIMP)-1, and superoxide dismutase(SOD) in H292 cells stimulated with LPS or CSE. Their related transcription factors and signaling pathways were also analyzed.RESULTS: BJF, BYF, and YZF significantly inhibited the LPS-or CSE-induced expressions of TNF-α, IL-8,MMP-9, TIMP-1, and SOD in H292 cells, and suppressed the activation of transcription factors including nuclear transcription factor(NF)-κB, activator protein(AP)-1, and signal transducers and activators of transcription(STAT) 3 and their corresponding pathways, including NF-κB, mitogen-activated protein kinase(MAPK), STAT3, and peroxisome proliferator-activated receptor(PPAR).CONCLUSION: BJF, BYF, and YZF effectively suppressed inflammatory responses, protease-antiprotease imbalance, and oxidative stress induced by LPS and CSE, an effect that was closely associated with the inhibition of the NF-κB, MAPK, STAT3, and PPAR pathways.展开更多
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)
文摘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Supported by National Natural Science Fund of China(No.81130062,81603473,81403367)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)。
文摘OBJECTIVE: To investigate the therapeutic efficacy of Tiaobu Feishen formulae(TBFS) on cigarette smoke-induced inflammation in vitro using lipopolysaccharide(LPS)-induced and cigarette smoke extract(CSE)-induced NCI-H292 cells.METHODS: We evaluated the inhibitory effects of Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF) on the expressions of inflammatory cytokines including tumor necrosis factor(TNF)-α and interleukin(IL)-8, matrix metalloproteinase(MMP)-9, tissue inhibitor of matrix metalloprotease(TIMP)-1, and superoxide dismutase(SOD) in H292 cells stimulated with LPS or CSE. Their related transcription factors and signaling pathways were also analyzed.RESULTS: BJF, BYF, and YZF significantly inhibited the LPS-or CSE-induced expressions of TNF-α, IL-8,MMP-9, TIMP-1, and SOD in H292 cells, and suppressed the activation of transcription factors including nuclear transcription factor(NF)-κB, activator protein(AP)-1, and signal transducers and activators of transcription(STAT) 3 and their corresponding pathways, including NF-κB, mitogen-activated protein kinase(MAPK), STAT3, and peroxisome proliferator-activated receptor(PPAR).CONCLUSION: BJF, BYF, and YZF effectively suppressed inflammatory responses, protease-antiprotease imbalance, and oxidative stress induced by LPS and CSE, an effect that was closely associated with the inhibition of the NF-κB, MAPK, STAT3, and PPAR pathways.
