Citrus alkaline extracts prevent fibroblast senescence to ameliorate pulmonary fibrosis via activation of COX-2 was written by Feng, Fanchao;Wang, Zhichao;Li, Ruofei;Wu, Qi;Gu, Cheng;Xu, Yong;Peng, Wenpan;Han, Di;Zhou, Xianmei;Wu, Jing;He, Hailang. And the article was included in Biomedicine & Pharmacotherapy in 2019.Formula: C16H19BrN2OS The following contents are mentioned in the article:
Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal lung disease with a poor prognosis and limited treatment options. The incidence of IPF increases with age, and the mechanisms related to aging such as cellular senescence have been strongly implicated in disease pathol. Therefore, a better understanding of fibroblasts senescence might provide a new therapeutic strategy to prevent and treat pulmonary fibrosis. In this study, we aimed to explore the effects of citrus alk. extracts (CAE) on the fibroblasts senescence, and elucidate the underlying mechanism to ameliorate pulmonary fibrosis. We demonstrated that CAE mitigated the collagen deposition by the initial early treatment, suggesting a potential preventive effect of CAE on pulmonary fibrosis. The expression of senescence biomarkers P16INK4a and P21, concomitant with down-regulation of the myofibroblasts marker α-SMA, and the number of senescence-associated β-galactosidase (SA-β-Gal) pos. cells were decreased by CAE treatment, indicating a significant inhibitory effect of CAE on fibroblast senescence. Addnl., CAE down-regulated the expression of the senescence-associated secretory phenotype (SASP) in etoposide-induced senescent fibroblasts. Further studies indicated that COX-2 activation was required for CAE to inhibit the lung fibroblast senescence through a P53-dependent pathway. Results showed that the anti-senescence effect of CAE was abrogated when COX-2 was knocked down or inhibited by COX-2 inhibitor NS-398 or indomethacin in lung fibroblasts. Meanwhile, the anti-fibrotic and anti-senescence effect of CAE were abolished due to disruption of COX-2 in vivo. Collectively, our results provided a novel insight into the potential mechanism of CAE to inhibit the fibroblasts activation through preventing cellular senescence. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Formula: C16H19BrN2OS).
2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles frequently appear in peptide studies. Thiazoles can also be used as protected formyl groups, which can be released in later stages of complex natural product synthesis. Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.Formula: C16H19BrN2OS
Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica