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ZHANG Tian-Zhu, YANG Shi-Hai, YAO Jin-Fu, DU Juan, YAN Tian-hua. Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway[J]. 中国天然药物, 2015, 13(12): 889-895.
引用本文: ZHANG Tian-Zhu, YANG Shi-Hai, YAO Jin-Fu, DU Juan, YAN Tian-hua. Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway[J]. 中国天然药物, 2015, 13(12): 889-895.
ZHANG Tian-Zhu, YANG Shi-Hai, YAO Jin-Fu, DU Juan, YAN Tian-hua. Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway[J]. Chinese Journal of Natural Medicines, 2015, 13(12): 889-895.
Citation: ZHANG Tian-Zhu, YANG Shi-Hai, YAO Jin-Fu, DU Juan, YAN Tian-hua. Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway[J]. Chinese Journal of Natural Medicines, 2015, 13(12): 889-895.

Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway

Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway

  • 摘要: In the present study, we investigated anti-inflammatory effects of Sangxingtang (SXT) on acute lung injury using a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid (BALF) was performed. The degree of lung edema was evaluated by measuring the wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor- (TNF-) and interleukin-6 (IL-6), were assayed by the enzyme-linked immunosorbent assay methods. Pathological changes of lung tissues were observed by Hematoxylin and eosin (HE) staining. The inflammatory signaling pathway-related proteins nuclear factor mitogen activated protein kinases (P38MAPK), extracellular regulated protein kinases (Erk), c-Jun N-terminal kinase (Jnk) and nuclear transcription factor (NF-B) p65 expressions were measured by Western blotting. Our results showed that the treatment with the SXT markedly attenuated the inflammatory cell numbers in the BALF, decreased the levels of P-P38MAPK, P-Erk, P-Jnk and P-NF-B p65 and the total protein levels in lungs, improved the SOD activity and inhibited the MPO activity. Histological studies demonstrated that SXT substantially reduced the LPS-induced neutrophils in lung tissues, compared with the untreated LPS group. In conclusion, our results indicated that SXT had protective effects on LPS-induced ALI in mice.

     

    Abstract: In the present study, we investigated anti-inflammatory effects of Sangxingtang (SXT) on acute lung injury using a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid (BALF) was performed. The degree of lung edema was evaluated by measuring the wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor- (TNF-) and interleukin-6 (IL-6), were assayed by the enzyme-linked immunosorbent assay methods. Pathological changes of lung tissues were observed by Hematoxylin and eosin (HE) staining. The inflammatory signaling pathway-related proteins nuclear factor mitogen activated protein kinases (P38MAPK), extracellular regulated protein kinases (Erk), c-Jun N-terminal kinase (Jnk) and nuclear transcription factor (NF-B) p65 expressions were measured by Western blotting. Our results showed that the treatment with the SXT markedly attenuated the inflammatory cell numbers in the BALF, decreased the levels of P-P38MAPK, P-Erk, P-Jnk and P-NF-B p65 and the total protein levels in lungs, improved the SOD activity and inhibited the MPO activity. Histological studies demonstrated that SXT substantially reduced the LPS-induced neutrophils in lung tissues, compared with the untreated LPS group. In conclusion, our results indicated that SXT had protective effects on LPS-induced ALI in mice.

     

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