1.Chemical constituents from the leaves of Anisopus mannii and the melanogenesis inhibitory activities
Feng YE ; Qinglin LYU ; Wanfang ZHU ; Feng FENG ; Jie ZHANG
Journal of China Pharmaceutical University 2018;49(6):676-681
The phytochemical studies on the leaves of Anisopus mannii led to the isolation of seven compounds by silica gel, ODS, DIAION HP-20, Sephadex LH-20 colunmn chromatographer, their structures were elucidated on the basis of the spectroscopic analyses(NMR, HRMS)and the comparisons with the literatures as 3β-acetoxylup-20(29)-ene(1), 1-acetoxy-2-isopropyl-1-tridecene(2), rutin(3), 3, 6′-diferuloylsucrose(4), 3-O-β-D-glucopyranosyl-3-β-hydroxyolean-12-en-28-oic acid 28-O-[α-L-rhamnopyra- nosyl-(1→2)-β-D-glucopyranosyl] ester(5), conduritol A(6), hoyacarnoside I(7). Meanwhile, the isolated compounds were evaluated for their inhibitory activities against melanogensis in B16 melanoma cells, as the results, all compounds exhibited melanogenesis-inhibitory activity and compound 5 showed a strongest activity(Melanin content: (27. 4±3. 5)%, Cell Viability: (54. 9±5. 6)% with a concentration of 30 μmol/L)which could be further developed.
2. Effects of sustained lung inflation combined with pulmonary surfactant on neonatal respiratory distress syndrome: a prospective randomized controlled trial
Junyan ZHONG ; Haifeng ZONG ; Nan YE ; Mei HUANG ; Yurong YUAN ; Sue ZHANG ; Wanfang ZHANG ; Lin ZHU ; Shujuan ZHANG ; Zhifeng HUANG ; Yuping SHI ; Chuanzhong YANG
Chinese Journal of Perinatal Medicine 2019;22(11):781-786
Objective:
To investigate the efficacy and adverse effects of sustained lung inflation (SLI) combined with pulmonary surfactant (PS) in the treatment of neonatal respiratory distress syndrome (NRDS).
Methods:
This prospective randomized controlled trial included 124 premature infants (gestational age <34 weeks and birth weight <2 000 g) diagnosed with NRDS and in need of PS treatment in Shenzhen Maternity & Child Healthcare Hospital affiliated to Southern Medical University from July 1, 2016 to October 31, 2018. They were randomly divided into experimental or control group, with 62 cases in each. Infants in the experimental group were treated with SLI using T-piece and intratracheal PS, while those in the control group were given PS only. Blood gas analysis and measurement of fraction of inspiration O2 (FiO2) and ratio of partial pressure of oxygen (PO2) over FiO2 were performed before and 1 h after PS injection. Results of the treatments and incidence of complications were compared. Paired samples
3.The lncSIL molecule exerts a negative regulatory effect on the alveolar epithelial-mesenchymal transition induced by TGF-β1 through modulation of the EZH2/P21/CDK6 signaling pathway
Wanfang Zhang ; Lin Wang ; Pengtao Pan ; Wenxin Li ; Ruili Kang ; Ziren Zhu ; Haoqin Chen ; Xinyu Fang ; Xingcan Zhang ; Yuxin Zhang ; Yiwen Jiang ; Xinyan Li ; Benqi Yuan
Acta Universitatis Medicinalis Anhui 2024;59(4):600-604
Objective :
To investigate the role of lncSIL in transforming growth factor-β1(TGF-β1)-induced alveo- lar epithelial interstitial transformation (EMT) and its related signaling pathways .
Methods :
Western blot was used to detect the effect of lncSIL silencing on the expression of E-cadherin ( E-cad) , alpha-smooth muscle actin ( α- SMA) and Collagen I (Col I) in the process of EMT induced by TGF-β1 . LncSIL interacting proteins were ana- lyzed by RNA pulldown . Western blot was used to detect the effect of overexpression or silencing of lncSIL on the expression of its target gene enhancer of zeste homolog 2 (EZH2) and its downstream factors P21 and cyclin-de- pendent kinase 6 (CDK6) . Flow cytometry was used to analyze the effect of lncSIL on cell cycle progression .
Results:
After lncSIL silencing , the expression of α-SMA and Col I increased , the expression of E-cad decreased . RNA pulldown assay showed that EZH2 was the target protein that interacted with lncSIL , and the expression of EZH2 increased after silencing lncSIL , the expression of EZH2 downstream gene P21 decreased , CDK6 increased . Flow cytometry showed that the number of cells in S phase significantly increased . When lncSIL was overexpressed , the expression of EZH2 and CDK6 was down-regulated , the expression of P21 was up-regulated , and the number of S phase cells significantly decreased .
Conclusion
LncSIL inhibits TGF-β1-induced alveolar epithelial cell mesen- chymal transition by negatively regulating EZH2/P21 /CDK6 signaling pathway to inhibit cell cycle progression .