作者机构：
[Wu, Di] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China;[Chen, Linxi] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China lxchen6@126.com
通讯机构：
[Chen, L.] I;Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China
关键词：
novel;promising;diseases
摘要：
Recently, Friedmann Angeli et al. [1] reported that the loss of ferroptosis regulation enzyme glutathione peroxidase 4 (GPX4) will cause an overwhelming ferroptosis of renal cells, which eventually induces renal failure. Yet, liproxstatin-1, a novel potent ferroptosis inhibitor, is able to alleviate tissue injury of ischemia/reperfusion-induced renal injury. This study smartly expanded the research on nonapoptotic cell death, ferroptosis, as researchers were just focused on its effect on tumor and neuronal diseases before [2,3]. Actually, ferroptosis is related to multiple pathophysiological processes, and triggering or inhibiting ferroptosis will be novel therapy strategies for many diseases, such as atherosclerosis, angiocardiopathy, and diabetes. In their research, the complex lipid oxidation was also investigated, which provided new possibilities for redox-target therapy [1].
作者机构：
[Zhao Q.; Sun Y.-Q.] Department of Pathology, First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China;[Chen P.] Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan 421001, China
通讯机构：
[Sun, Y.-Q.] D;Department of Pathology, First Affiliated Hospital, University of South China, Hengyang, Hunan, China
摘要：
RIMARY pulmonary sarcomatoid carcinoma (PSC) is a rare condition, approximately accounting for 0.1%-0.4% of all lung malignancies. PSCs consist of 5 major histological variants according to 2004 WHO classification:pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma. PSC patients are predominantly male smokers with an average age of 65 years at diagnosis. Carcinosarcoma is a biphasic tumor characterized by an admixture of both malignant epithelial and mesenchymal components as in well-defined carcinomas and sarcomas. In this article, we reported a rare female case of pulmonary carcinosarcoma with intracardiac extension.
作者机构：
[刘彦梅; 骆镜妃; 郭锋; 全海燕; 彭虹艳] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China;[秦旭平] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China. qinxuping@sohu.com
作者机构：
[张秀芹; 黄红林; 汪煜华; 李冬花] Learning Key Laboratory for Pharmacoproteomics of Hunan Province, Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan, 421001, China;Loudi Health School, Loudi Hunan, 417000, China;[刘玉玲] Learning Key Laboratory for Pharmacoproteomics of Hunan Province, Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan, 421001, China, Loudi Health School, Loudi Hunan, 417000, China
作者机构：
[Zhang Cai-Ping] Univ South China, Coll Med, Hengyang 421001, Peoples R China.;[Lin Li-Mei; Tuo Qin-Hui; Sun Shao-Wei; Gong Yong-Zhen; Liao Duan-Fang] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Div Stem Cell Regulat & Applicat, Changsha 410205, Hunan, Peoples R China.;[Zhang Cai-Ping; Zheng Xing; Sun Shao-Wei; Ou Lu; Lei Xiao-Yong] Univ South China, Coll Pharm & Biol Sci, Hengyang 421001, Peoples R China.;[Tuo Qin-Hui; Gong Yong-Zhen; Liao Duan-Fang] Hunan Univ China, Sinoluxembourg Cooperat Res Ctr Chinese Med, Med, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Liao Duan-Fang] H;Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Div Stem Cell Regulat & Applicat, Changsha 410205, Hunan, Peoples R China.
摘要：
The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcinoma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B (LC3A/B), and beclin1, and confirmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. Moreover, there are pores on the surface of human lung adenocarcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force microscopy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation.
摘要：
Aim: To investigate the mechanisms of anti-atherosclerotic action of ezetimibe in rat vascular smooth muscle cells (VSMCs) in vitro. Methods: VSMCs of SD rats were cultured in the presence of Chol:MβCD (10 μg/mL) for 72 h, and intracellular lipid droplets and cholesterol levels were evaluated using Oil Red O staining, HPLC and Enzymatic Fluorescence Assay, respectively. The expression of caveolin-1，sterol response element-binding protein-1 (SREBP-1) and ERK1/2 were analyzed using Western blot assays. Translocation of SREBP-1 and ERK1/2 was detected with immunofluorescence. Results: Treatment with Chol: MβCD dramatically increased the cellular levels of total cholesterol (TC)，cholesterol ester (CE) and free cholesterol (FC) in VSMCs, which led to the formation of foam cells. Furthermore, Chol:MβCD treatment significantly decreased the expression of caveolin-1, and stimulated the expression and nuclear translocation of SREBP-1 in VSMCs. Co-treatment with ezetimibe (3 μmol/L) significantly decreased the cellular levels of TC, CE and FC, which was accompanied by elevation of caveolin-1 expression, and by a reduction of SREBP-1 expression and nuclear translocation. Co-treatment with ezetimibe dose-dependently decreased the expression of phosphor-ERK1/2 (p-ERK1/2) in VSMCs. The ERK1/2 inhibitor PD98059 (50 μmol/L) altered the cholesterol level and the expression of p-ERK1/2, SREBP-1 and caveolin-1 in the same manner as ezetimibe did. Conclusion: Ezetimibe suppresses cholesterol accumulation in rat VSMCs in vitro by regulating SREBP-1 and caveolin-1 expression, possibly via the MAPK signaling pathway.
