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Capsaicin으I PDGF-BB에 의한 간 성상세포 증식 및 활성 억제효과
이기호, 진순우, 정혜광 충남대학교 약학대학 의약품개발연구소 2017 藥學論文集 Vol.32 No.-
During the process of liver fibrosis, hepatic stellate cells (HSCs) play a critical role in the increased formation and reduced degradation of extracellular matrix in the liver. Capsaicin (CPS) exerts many pharmacological effects. but any possible influence on HSCs remains unclear. Therefore. we evaluated the in-hibitory effects of CPS on Platelet-derived growth factor(PDGF)-BB-induced hepatic stellate cells (HSCs) proliferation and activation. The CPS suppressed HSC activation. including PDGF-BB-induced proliferation. u -smooth muscle actin (a-SMA) expression and collagen accumulation. Additionally, CPS inhibited PDGF-BB-induced Akt and ERK1/2 phosphorylation. Furthermore, in HSCs, CPS inhibited the PDGF-BB-in-duced increases in a一SMAand collagen type 1 expression. via Akt and ERK1/2 inhibition. These results in-dicate that CPS can ameliorate hepatic fibrosis by inhibiting the Akt and ERK1/2 pathway.
Tetrabromobisphenol A가 인간 유방암 세포 MCF-7에서 Fatty Acid Synthase 발현에 미치는 영향
김지연, 이기호, 진순우, 정혜광 충남대학교 약학대학 의약품개발연구소 2021 藥學論文集 Vol.36 No.-
Breast cancer is the most common malignant cancer and the major cause of mortality due to cancer in females worldwide, and the morbidity has increased gradually over recent years. Cancer cells require more energy and nutrients than normal cells for rapid growth and proliferation, which can be satisfied from lipids. Therefore, lipogenesis occurs more actively in cancer cells. In previous studies, fatty acid synthase (FASN) overexpression in breast cancer patients was found to be a poor prognostic factor for disease, suggesting the possibility of FASN inhibitor as a drug target in breast cancer treatment. protein kinase B (Akt) and AMP-activated protein kinase (AMPK) were reported to regulate sterol regulatory element-binding protein-1c (SREBP-1c) which is transcription facfor of FASN. Tetrabromobisphenol A (TBBPA), the most common industrial brominated flame retardant, acts as a cytotoxic, neurotoxic, and immunotoxicant, causing inflammation. However, despite the harmful effects of TBBPA, the effects and mechanisms of TBBPA on fatty acid synthesis in breast cancer cells are unclear. Therefore, this study investigated the effect of TBBPA on fatty acid synthesis in breast cancer cells. In human breast cancer MCF-7 cells, treatment with TBBPA significantly induced the expression of FASN and SREBP-1c. Furthermore, TBBPA induced phosphorylation of Akt and suppressed phosphorylation of AMPK. Taken together, these results suggest that TBBPA may induce lipid synthesis by regulating SREBP-1c via Akt and AMPK signaling pathway in breast cancer MCF-7 cells.