In the present study, we aimed to investigate the effects of Xiao-Xu-Ming decoction extract(XXM) on lipopolysaccaride(LPS)-induced neuroinflammation in vitro and in vivo. In vitro, the microglia BV2 cells were treated...In the present study, we aimed to investigate the effects of Xiao-Xu-Ming decoction extract(XXM) on lipopolysaccaride(LPS)-induced neuroinflammation in vitro and in vivo. In vitro, the microglia BV2 cells were treated with 200 ng/mL LPS for 24 h to induce inflammatory responses. In vivo, mice were treated with 5 mg/kg LPS to induce inflammatory responses. The NO level was determined by Griess Reagents. The levels of IL-1β, IL-6, TNF-α and MCP-1 were determined by ELISA. The expressions of Iba-1, TLR4 and MyD88 at the protein levels were determined by Western blotting analysis. The mRNA levels of TLR4 and MyD88 were determined by real-time PCR. In vitro, XXM significantly reduced the levels of various pro-inflammatory factors, including NO, IL-1β, IL-6 and TNF-α, induced by LPS in the supernatant of BV2 cells and suppressed expressions of inflammatory proteins TLR4 and MyD88 induced by LPS in BV2 cells. In vivo, XXM significantly inhibited microglia activation, attenuated LPS-induced inflammatory factors and chemokine production, such as IL-1β, IL-6, TNF-α and MCP-1, and inhibited the expressions of inflammatory proteins including TLR4 and MyD88, in the cortex of LPS-induced mice. Our findings suggested that XXM could attenuate LPS-induced neuroinflammation via down-regulating TLR4/MyD88 signaling pathway.展开更多
Acute kidney injury(AKI)is a common clinical serious illness.Esculin(ES)is a coumarin compound of traditional Chinese medicine Cortex Fraxini.Our previous study has found that ES protects against inflammation and rena...Acute kidney injury(AKI)is a common clinical serious illness.Esculin(ES)is a coumarin compound of traditional Chinese medicine Cortex Fraxini.Our previous study has found that ES protects against inflammation and renal damage in diabetic rats.In the present study,we aimed to investigate the effects and the possible mechanism of ES against lipopolysaccharides(LPS)-induced AKI in mice.Renal morphology was observed by H&E staining.Renal function was evaluated by blood urea nitrogen(BUN)level and creatinine content in serum.Inflammatory factor levels were measured by ELISA assay.The inflammatory proteins were analyzed by RT-PCR and Western blotting analysis.The results showed that ES alleviated LPS-induced pathological injury and renal dysfunction,and decreased BUN level and creatinine content in serum.In addition,ES significantly reduced the release of pro-inflammatory factors,including IL-1β,IL-6 and TNF-α,chemokine MCP-1 and cell adhesion molecule ICAM-1.Furthermore,the expressions of inflammatory pathway proteins P2 X7,HMGB1,TLR4 and MyD88 both at the mRNA and protein levels were all down-regulated by ES in the kidney tissue of LPS-challenged mice.These results suggested ES protected against LPS-induced AKI through inhibiting P2 X7 expression and HMGB1/TLR4 inflammatory pathway.展开更多
基金The National Natural Science Foundation of China(Grant No.81473383)the Innovation Fund for Graduate of Beijing Union Medical College(Grant No.2017-1007-02)+1 种基金the Drug Innovation Major Project(Grant No.2018ZX09711001-003-019)the Medical and Health Innovation Project of Chinese Academy of Medical Sciences(Grant No.2016-I2M-3-007,2018-1007-04)
文摘In the present study, we aimed to investigate the effects of Xiao-Xu-Ming decoction extract(XXM) on lipopolysaccaride(LPS)-induced neuroinflammation in vitro and in vivo. In vitro, the microglia BV2 cells were treated with 200 ng/mL LPS for 24 h to induce inflammatory responses. In vivo, mice were treated with 5 mg/kg LPS to induce inflammatory responses. The NO level was determined by Griess Reagents. The levels of IL-1β, IL-6, TNF-α and MCP-1 were determined by ELISA. The expressions of Iba-1, TLR4 and MyD88 at the protein levels were determined by Western blotting analysis. The mRNA levels of TLR4 and MyD88 were determined by real-time PCR. In vitro, XXM significantly reduced the levels of various pro-inflammatory factors, including NO, IL-1β, IL-6 and TNF-α, induced by LPS in the supernatant of BV2 cells and suppressed expressions of inflammatory proteins TLR4 and MyD88 induced by LPS in BV2 cells. In vivo, XXM significantly inhibited microglia activation, attenuated LPS-induced inflammatory factors and chemokine production, such as IL-1β, IL-6, TNF-α and MCP-1, and inhibited the expressions of inflammatory proteins including TLR4 and MyD88, in the cortex of LPS-induced mice. Our findings suggested that XXM could attenuate LPS-induced neuroinflammation via down-regulating TLR4/MyD88 signaling pathway.
基金The National Key Research&Development Plan(Grant No.2018YFC0311005)the National Natural Science Foundation of China(Grant No.81473383)+2 种基金the Significant New-Drugs Creation of Science and Technology Major Projects(Grant No.2012ZX09103101-078)the Medical and Health Innovation Project of Chinese Academy of Medical Sciences(Grant No.2016-I2M-3-007)Innovation Fund for Doctoral Students of Beijing Union Medical College(Grant No.2018-1007-04).
文摘Acute kidney injury(AKI)is a common clinical serious illness.Esculin(ES)is a coumarin compound of traditional Chinese medicine Cortex Fraxini.Our previous study has found that ES protects against inflammation and renal damage in diabetic rats.In the present study,we aimed to investigate the effects and the possible mechanism of ES against lipopolysaccharides(LPS)-induced AKI in mice.Renal morphology was observed by H&E staining.Renal function was evaluated by blood urea nitrogen(BUN)level and creatinine content in serum.Inflammatory factor levels were measured by ELISA assay.The inflammatory proteins were analyzed by RT-PCR and Western blotting analysis.The results showed that ES alleviated LPS-induced pathological injury and renal dysfunction,and decreased BUN level and creatinine content in serum.In addition,ES significantly reduced the release of pro-inflammatory factors,including IL-1β,IL-6 and TNF-α,chemokine MCP-1 and cell adhesion molecule ICAM-1.Furthermore,the expressions of inflammatory pathway proteins P2 X7,HMGB1,TLR4 and MyD88 both at the mRNA and protein levels were all down-regulated by ES in the kidney tissue of LPS-challenged mice.These results suggested ES protected against LPS-induced AKI through inhibiting P2 X7 expression and HMGB1/TLR4 inflammatory pathway.
