Mechanism of Shaoyaotang in Treatment of Ulcerative Colitis Based on Network Pharmacology and Experimental Verification / 中国实验方剂学杂志

ObjectiveTo explore the mechanism of Shaoyaotang （SYT） in the treatment of ulcerative colitis （UC） based on network pharmacology and experimental verification. MethodThe core components， target genes， and main pathways of SYT were predicted based on network pharmacology， and UC-related components， target genes， and pathways were screened. Dextran sodium sulfate （DSS） was used to induce the UC model in mice， and the effect of SYT on UC mice was observed， followed by mechanism verification. ResultNetwork pharmacology indicated that 174 active components and corresponding 159 target genes of SYT were screened， and the related pathways were those mediated by 5-hydroxytryptamine （5-HT） degredation and 5-HT receptor 3. The results of animal experiments showed that compared with the model group， the SYT group showed increased body weight and colon length（P<0.01）， reduced disease activity index （DAI） score （P<0.01）， improved histopathological manifestations， reduced concentrations of 5-HT in the colonic tissues and serum （P<0.05， P<0.01）， and increased mRNA expression of monoamine oxidase A （MAOA）， monoamine oxidase B （MAOB）， sodium-dependent serotonin transporter （SLC6A4）， and 5-HT receptor 3A （5-HTR3A） related to 5-HT metabolism in the colon （P<0.01）. ConclusionSYT can alleviate the local inflammatory response of the intestinal tract in UC by regulating 5-HT degredation pathways.

Anti-inflammatory Effect of the Luteolin-4, 4' -dipyridy Co-crystal on Macrophage RAW264.7 in Mice / 中国药房

OBJECTIVE: To study anti-inflammatory effect and mechanism of the luteolin · 4, 4' -dipyridy co-crystal.METHODS: Using macrophage RAW264. 7 of normal mice as control, the inflammation model was established with lipopolysaccharide (LPS) -induced RAW264. 7 cells. MTT assay was used to detect cells activity 2 h after treatment of different concentrations of luteolin (10, 20, 40, 80 μmol/L), 4, 4' -dipyridy (10,20, 40,80 μmol/L) and luteolin·4, 4' -dipyridy co-crystal (10, 20, 40, 80 μmol/L). The mRNA expression of iNOS and COX-2 in RAW264. 7 cells at 40 μmol/L were determined by qRT-PCR. The protein expression of TNF-α and IL-6 in RAW264. 7 cells at 40 μmol/L were determined by ELISA. The protein expression of NF-κB p65 in RAW264. 7 cells at 40 μmol/L were determined by Western bolt. RESULTS: Compared with normal cells, the activity of RAW264. 7 cells was decreased significantly after induced by LPS (P<0. 01); mRNA expression of iNOS and COX-2, protein expression of TNF-α, IL-6 and NF-κB p65 were increased significantly (P<0. 01). Both luteolin and luteolin · 4, 4' -dipyridy co-crystal could enhance the activity of RAW264. 7 cells after induced by LPS (P<0. 05 or P<0. 01) in concentration-dependent manner. 4, 4' -dipyridy had no significant effect on the activity of RAW264. 7 cells after induced by LPS. After luteolin and luteolin· 4, 4' -dipyridy co-crystal at 40 μmol/L, mRNA expression of iNOS and COX-2, protein expression of TNF-α, IL-6 and NF-κB p65 in RAW264. 7 cells after induced by LPS were decreased significantly (P<0. 05 or P<0. 01); the luteolin · 4, 4' -dipyridy co-crystal was better than luteolin (P<0. 05 or P<0. 01). CONCLUSIONS: The luteolin·4, 4' -dipyridy co-crystal can inhibit the generation of inflammatory factors by down-regulating NF-κB signal, and its anti-i nflammatory effect is better than luteolin.