title: Catalpol modulates the expressions of Bcl-2 and Bax and attenuates apoptosis in gerbils after ischemic injury.
abstract: Our previous study described the neuroprotective effects of catalpol in gerbil ischemic model, in which catalpol was shown to prevent hippocampal neurons from death and ameliorate the cognitive ability of the animals. In the study, we focused on investigating the neuroprotective mechanism of catalpol. Animals were randomly assigned three groups as sham-operated, ischemia-treated with saline and ischemia-treated with catalpol. Transient global ischemia was produced by a 5 min occlusion of the bilateral common carotid arteries. Catalpol was intraperitoneally injected at the dose of 5 mg/kg immediately after reperfusion and repeatedly at 12, 24, 48 and 72 h. Histology as well as immunohistochemistry and TUNEL (the terminal deoxynucleotidyl transferase-mediated UTP nick end label) analysis were performed on serial slices through the dorsal hippocampus after gerbils were sacrificed. The results showed that 5 min transient global ischemia followed by 4 days reperfusion caused significant increases in TUNEL-positive and Bax-positive cells in hippocampal CA1 subfield. Catalpol not only significantly reduced TUNEL-positive and Bax-positive cells but also significantly increased Bcl-2-positive cells. All these suggested that catalpol could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes.
authors.affiliation: The Second Affiliated Hospital, Dalian Medical University, Dalian, Liaoning 116023, PR China. Li.lyl_lhc@163.com <Li.lyl_lhc@163.com>
authors.forename: Dan-Qing
authors.initials: DQ
authors.lastname: Li
authors.forename: Yong-Ming
authors.initials: YM
authors.lastname: Bao
authors.forename: Yang
authors.initials: Y
authors.lastname: Li
authors.forename: Cheng-Fang
authors.initials: CF
authors.lastname: Wang
authors.forename: Yuxin
authors.initials: Y
authors.lastname: Liu
authors.forename: Li-Jia
authors.initials: LJ
authors.lastname: An
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D020520:Brain Infarction / Q000188:drug therapy / Q000201:enzymology / Q000503:physiopathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000201:enzymology / Q000503:physiopathology; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D004365:Drugs, Chinese Herbal / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology; D005849:Gerbillinae; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology / Q000503:physiopathology; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D057888:Iridoid Glucosides; D039823:Iridoids / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D009410:Nerve Degeneration / Q000188:drug therapy / Q000201:enzymology / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects* / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000201:enzymology / Q000503:physiopathology; D016896:Treatment Outcome; D051028:bcl-2-Associated X Protein / Q000187:drug effects* / Q000378:metabolism
chemical_list: D004365:Drugs, Chinese Herbal; D005960:Glucosides; D057888:Iridoid Glucosides; D039823:Iridoids; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C078040:catalpol