Components of drugs in acupoint sticking therapy and its mechanism of intervention on bronchial asthma based on UPLC-Q-TOF-MS combined with network pharmacology and experimental verification / 中国中药杂志

UPLC-Q-TOF-MS combined with network pharmacology and experimental verification was used to explore the mechanism of acupoint sticking therapy(AST) in the intervention of bronchial asthma(BA). The chemical components of Sinapis Semen, Cory-dalis Rhizoma, Kansui Radix, Asari Radix et Rhizoma, and Zingiberis Rhizoma Recens were retrieved from TCMSP as self-built database. The active components in AST drugs were analyzed by UPLC-Q-TOF-MS, and the targets were screened out in TCMSP and Swiss-TargetPrediction. Targets of BA were collected from GeneCards, and the intersection of active components and targets was obtained by Venny 2.1.0. The potential targets were imported into STRING and DAVID for PPI, GO, and KEGG analyses. The asthma model induced by house dust mite(HDM) was established in mice. The mechanism of AST on asthmatic mice was explored by pulmonary function, Western blot, and flow cytometry. The results indicated that 54 active components were obtained by UPLC-Q-TOF-MS and 162 potential targets were obtained from the intersection. The first 53 targets were selected as key targets. PPI, GO, and KEGG analyses showed that AST presumedly acted on SRC, PIK3 CA, and other targets through active components such as sinoacutine, sinapic acid, dihydrocapsaicin, and 6-gingerol and regulated PI3 K-AKT, ErbB, chemokine, sphingolipid, and other signaling pathways to intervene in the pathological mechanism of BA. AST can improve lung function, down-regulate the expression of PI3 K and p-AKT proteins in lung tissues, enhance the expression of PETN protein, and reduce the level of type Ⅱ innate immune cells(ILC2 s) in lung tissues of asthmatic mice. In conclusion, AST may inhibit ILC2 s by down-regulating the PI3 K-AKT pathway to relieve asthmatic airway inflammation and reduce airway hyperresponsiveness.

Stachydrine Inhibits the Growth of Colon Cancer by Regulating the Expression of ACTG2 / 中国药学杂志

OBJECTIVE: To investigate the effect of stachydrine on tumor growth of colon cancer and its mechanisms. METHODS: MTS was used to test the effect of stachydrine on proliferation of HCT116 colon cancer cell. HCT116 colon cancer xenograft model was used to detect the effect of stachydrine on tumor growth in vivo. Immunohistochemical was used to determine the effect of stachydrine on expression of smooth muscle actin 2 (ACTG2) in subcutaneous transplantation tumor. The transfection of ACTG2 siRNA into HCT116 cells was conducted to study the effect of ACTG2 intervene on tumor angiogenesis by tube formation experiment in colon cancer. The protein expression of VEGF, bFGF, TNF-α and PDGF after ACTG2 intervene were examined by Western blotting to explore the potential mechanisms of stachydrine on regulation of tumor angiogenesis. RESULTS: Compared with the control group, the proliferation and growth of HCT116 colon cancer cells were significant inhibited by stachydrine in vitro and in vivo. Immunohistochemical showed that the expression of ACTG2 was significantly decreased by treatment with stachydrine. ACTG2 siRNA transfection could significantly decreased the inhibition effect of stachydrine on tumor angiogenesis. Mechanistic study found that stachydrine could inhibit the expression of VEGF, bFGF, TNF-α and PDGF, however, ACTG2 siRNA transfection could significantly reverse the expression of above mentioned angiogenesis-related factors. CONCLUSION: Stachydrine could inhibit the growth of colon cancer by suppressing tumor angiogenesis, and such effect is dependent on ACTG2 expression.