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Effects of ghrelin on homocysteine‐induced dysfunction and inflammatory response in rat cardiac microvascular endothelial cells
Author(s) -
Wang Dongjuan,
Wang Haichang,
Luo Peng,
Hwang Andrew,
Sun Dongdong,
Wang Yabin,
Zhang Zheng,
Liu Nan,
Wang Shenxu,
Li Chengxiang,
Cao Feng
Publication year - 2012
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20110235
Subject(s) - ghrelin , enos , endocrinology , medicine , nitric oxide , homocysteine , secretion , proinflammatory cytokine , endothelial dysfunction , hmgb1 , apoptosis , nitric oxide synthase , western blot , endothelial stem cell , chemistry , biology , inflammation , hormone , biochemistry , in vitro , gene
Ghrelin is a well‐characterized hormone that has protective effects on endothelial cells. Elevated HCY (homocysteine) can be a cardiovascular risk factor, but it is not known whether ghrelin can inhibit HCY‐induced dysfunction and inflammatory response in rat CMECs (cardiac microvascular endothelial cells). We found that HCY treatment for 24 h inhibited proliferation and NO (nitric oxide) secretion, but with increased cell apoptosis and secretion of cytokines in CMECs. In contrast, ghrelin pretreatment significantly improved proliferation and NO secretion, and inhibited cell apoptosis and secretion of cytokines in HCY‐induced CMECs. In addition, Western blot assay showed that NF‐κB (nuclear factor κB) and cleaved‐caspase 3 expression were elevated, and PCNA (proliferating cell nuclear antigen) and eNOS (endothelial nitric oxide synthase) expression were decreased after treatment with HCY, which was significantly reversed by pretreatment with ghrelin. The data suggest that ghrelin inhibits HCY‐induced CMEC dysfunction and inflammatory response, probably mediated by inhibition of NF‐κB activation.