作者机构:
[王紫涵; 何剑琴; 凌宏艳; 罗金定; 杨丝丝; 李梦伟] Hengyang Medical College, University of South China, Dept of Physiology,, Hunan, Hengyang, 421001, China;Physical Education Institute, Jishou University, Xiangxi, Hunan416000, China;[丁星星] Chuanshan College University of Sowth China, Hunan, 421001, China;[奉水东] Public Health College, University of South China.Hengyang, Dept of Social Medicine and Health Management,, Hunan, 421001, China;[Lyu H.-J.] Hengyang Medical College, University of South China, Dept of Physiology,, Hunan, Hengyang, 421001, China, Physical Education Institute, Jishou University, Xiangxi, Hunan416000, China
作者机构:
[王晓亮; 彭国文] School of Chemistry and Chemical Engineering, University of South China, Hengyang, China;[杨锦然; 黄红; 周归] Wang Chuanshan College, University of South China, Hengyang, China;[彭国文] School of Resources and Safety Engineering, Central South University, Changsha, China;[胡南; 肖方竹; 彭国文; 丁德馨; 张志军] Key Discipline Laboratory for National Defence for Biotechnology in Uranium Mining and Hydrometallurgy, University of South China, Hengyang, China
通讯机构:
School of Chemistry and Chemical Engineering, University of South China, Hengyang, China
作者机构:
[Gu Hong-Feng] Univ South China, Dept Physiol, Hengyang 421001, Peoples R China.;[Gu Hong-Feng; Yang Yong-Zong] Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Peoples R China.;[Jiang Jian-Hong] Nanhua Univ, Chuanshan Coll, Hengyang 421001, Peoples R China.;[Tong Qiao-Zhen; Liao Duan-Fang] Hunan Univ Chinese Med, Div Stem Cell Regulat & Applicat, State Key Lab Chinese Med Powder & Med Innovat Hu, Changsha 410208, Hunan, Peoples R China.
通讯机构:
[Gu Hong-Feng] U;Univ South China, Dept Physiol, Hengyang 421001, Peoples R China.
关键词:
GP Ⅱb/Ⅲa;atherosclerosis;HMGB-1;TLR4;NF-κB
摘要:
The effects of glycoprotein (GP) Ⅱb/Ⅲa inhibitors on the development of the atherosclerotic process has received scant attention. To investigate whether GP Ⅱb/Ⅲa blockade influences atherosclerosis lesion and HMGB-1/TLR4 signaling, we compared plaque formation in ApoE~(-/-) mice: control group (n=10); IgG group (n=10, 50 μg) and GP Ⅱb/Ⅲa mAb group (n=10, 50 μg). All mice were fed on a Western diet (10% fat and 1.25% cholesterol) for 10 weeks. GP Ⅱb/Ⅲa blockade significantly decreased the atherosclerotic lesion and platelet adhesion to the vessel wall. Immunohistochemistry analysis showed that blocking GP Ⅱb/Ⅲa diminished MOMA-2 and VCAM-1 expression in aortic plaque in ApoE~(-/-) mice. Western blot results indicated that HMGB-1, TLR4, and NF-κB levels were markedly reduced in arteries of ApoE-/- mice treated with GP Ⅱb/Ⅲa mAb (P < 0.05). Moreover, GP Ⅱb/Ⅲa mAb decreased plasma HMGB-1, IL-1β, TNF-α and MCP-1 concentrations. Our findings demonstrated that GP Ⅱb/Ⅲa mAb significantly decreased atherosclerotic lesions and HMGB-1, TLR4 and NF-κB expression in ApoE~(-/-) mice (P < 0.05). The present study has suggested a possibility that GP Ⅱb/Ⅲa blockade attenuates atherosclerosis by inhibiting the HMGB-1/TLR4 pathway..