title: Tanshinone inhibits neuronal cell apoptosis and inflammatory response in cerebral infarction rat model.
abstract: We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). In addition, rat primary neuronal cells were isolated and cultured in oxygen-glucose deprivation (OGD) conditions. After pretreatment with TSN, cell viability and apoptosis were observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. The expressions of Bax and B-cell lymphoma 2 (Bcl-2) were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. Compared with untreated cerebral infarction rat, TSN treatment significantly reduced cerebral infarct volume, cerebral edema, and neurological deficits score ( P < 0.05). Cell apoptosis as well as the levels of IL-6, TNF-α, and CRP in hippocampus and cortex of cerebral infarction rat were inhibited after pretreatment with TSN ( P < 0.05). Furthermore, TSN remarkably increased cell viability and inhibited cell apoptosis ratio ( P < 0.05) in OGD-induced rat neuronal cells. Besides, TSN significantly downregulated the expression of Bax and upregulated Bcl-2 ( P < 0.05). TSN IIA has a preventive effect on cerebral infarction by inhibiting neuronal cell apoptosis and inflammatory response in vitro and in vivo.
authors.affiliation: 1 Department of Rehabilitation Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Zhou
authors.affiliation: 2 Department of Massage, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.affiliation: 1 Department of Rehabilitation Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Wang
authors.affiliation: 3 Department of Rehabilitation Medicine, The Second Hospital of Shandong University, Jinan, China.
authors.forename: Qiangsan
authors.initials: Q
authors.lastname: Sun
mesh_terms: D045784:Abietanes / Q000494:pharmacology* / Q000627:therapeutic use*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D045784:Abietanes; D015850:Interleukin-6; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; C021751:tanshinone; D002097:C-Reactive Protein
keywords: cell apoptosis; cerebral infarction; inflammatory response; tanshinone IIA