title: Paeonol Inhibits the Proliferation, Invasion, and Inflammatory Reaction Induced by TNF-α in Vascular Smooth Muscle Cells.
abstract: The aim of this study was to evaluate the effect of paeonol on the proliferation, migration, and inflammation induced by tumor necrosis factor (TNF-α) of rat vascular smooth muscle cells (VSMCs). Primary rat VSMCs were identified by immunofluorescence assay. The inhibition of VSMCs proliferation induced by TNF-α was observed after paeonol treatment in a dose-dependent manner. Treatment with 100 μM paeonol significantly reduced the expression of proliferating cell nuclear antigen (PCNA). On the other hand, transwell assay showed that treatment with paeonol suppressed the invasion of TNF-α-induced VSMCs and the production of inflammation factors stimulated by TNF-α. For apoptosis induced by paeonol, Western blot analysis showed that cleaved caspase-3 and -9 were detected, and pro-apoptotic protein Bax was up-regulated, whereas anti-apoptotic protein Bcl-2 was down-regulated by paeonol in TNF-α-stimulated VSMCs. ELISA analysis data showed that both levels of IL-1β and IL-6 produced by the stimulation of TNF-α were decreased by paeonol in a dose-dependent manner in VSMCs. These results suggest that paeonol can effectively inhibit the proliferation through apoptotic induction through caspase pathway in VSMCs induced by TNF-α. Also, paeonol significantly reduced the invasion and the inflammation stimulated by TNF-α in VSMCs.
authors.affiliation: Department of Circulation, The Central Hospital Affiliated to Shenyang Medical College, Shenyang, 110024, People's Republic of China.
authors.forename: Liang
authors.initials: L
authors.lastname: Meng
authors.affiliation: Department of Science and Education, The Central Hospital Affiliated to Shenyang Medical College, Shenyang, 110024, People's Republic of China.
authors.forename: Weidong
authors.initials: W
authors.lastname: Xu
authors.affiliation: Admission Office, The Central Hospital Affiliated to Shenyang Medical College, Shenyang, 110024, People's Republic of China.
authors.forename: Lihong
authors.initials: L
authors.lastname: Guo
authors.affiliation: Department of Pharmacy, The Central Hospital Affiliated to Shenyang Medical College, Shenyang, 110024, People's Republic of China.
authors.forename: Wenqi
authors.initials: W
authors.lastname: Ning
authors.affiliation: Department of General Surgery, The Central Hospital Affiliated to Shenyang Medical College, 5 West Nanqi Road, Shenyang, 110024, People's Republic of China. zeng_xiandong@126.com.
authors.forename: Xiandong
authors.initials: X
authors.lastname: Zeng
mesh_terms: D000098:Acetophenones / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D053583:Interleukin-1beta / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000098:Acetophenones; D053583:Interleukin-1beta; D015850:Interleukin-6; D018809:Proliferating Cell Nuclear Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; C013638:paeonol; D053148:Caspase 3; D053453:Caspase 9; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9
keywords: Apoptosis; Cell proliferation; Invasion and inflammation; Paeonol; TNF-α; Vascular smooth muscle cells (VSMCs)