期刊：
Clinical and Experimental Pharmacology and Physiology,2009年36(9):e32-e39 ISSN：0305-1870
通讯作者：
Liao, Duan-Fang
作者机构：
[Ling, Hong-Yan; Liao, Duan-Fang] Cent S Univ, Dept Pharmacol, Sch Pharmaceut Sci, Changsha, Hunan, Peoples R China.;[Tang, Cao-Ke; Zhang, Liang; Yin, Wei-Dong; Liao, Duan-Fang] Univ S China, Res Ctr Life Sci, Key Lab Atherosclerol Hunan Prov, Hengyang 421001, Hunan, Peoples R China.;[Chen, Lin-Xi; Gao, Zhi-Ping; Zhang, Xiao-Ying; Zhu, Bing-Yang; Ou, He-Sheng; Ling, Hong-Yan; Tuo, Qin-Hui; Liao, Duan-Fang] Univ S China, Res Ctr Life Sci, Key Lab Pharmacoprote Hunan Prov, Inst Pharm & Pharmacol, Hengyang 421001, Hunan, Peoples R China.;[Ling, Hong-Yan] Univ S China, Res Ctr Life Sci, Dept Physiol, Sch Med, Hengyang 421001, Hunan, Peoples R China.;[Feng, Shui-Dong] Univ S China, Res Ctr Life Sci, Sch Publ Hlth, Dept Epidemiol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Liao, Duan-Fang] U;Univ S China, Res Ctr Life Sci, Key Lab Atherosclerol Hunan Prov, 28 W Chengsheng Rd, Hengyang 421001, Hunan, Peoples R China.
摘要：
Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular and nervous systems. Importantly, APJ is also involved in the pathogenesis if HIV-1 infection. We investigated whether vascular smooth muscle cell proliferation was regulated through an apelin-pERK1/2-cyclin D1 signal transduction pathway. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation and increased cell cycle progression. Apelin-13 a decreased the proportion of cell in the G0/G1 phase while increasing the number of cells in S phase. Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2. Treatment of cells with the MEK inhibitor PD98059 attenuated the apelin-3-induced pERK1/2 activation. Similarly, treatment with PD98059 partially diminished the apelin-13-induced expression of cyclin D1 and vascular smooth muscle cell proliferation. Taken together, these data established that apelin-13 stimulates vascular smooth muscle cell proliferation by promoting the G1-S phase transition, and that this effect is mediated in part by an apelin-pERKl/2-cyclin D1 signal cascade.
通讯机构：
[Pan, W.-N.] I;Institute of Pharmacy and Pharmacology, University of South China, China
关键词：
血管平滑肌细胞;细胞周期蛋白
摘要：
目的研究G蛋白偶联受体APJ（血管紧张素受体样受体或称血管紧张素受体AT．相关的受体蛋白，putative receptor protein related to the angiotensinreceptor AT_1）的内源性配体apelin-13通过PKC—ERK1／2-Cyclins信号通路促进大鼠血管平滑肌细胞（vascular smooth muscle cells，VSMCs）增殖的影响。方法培养SD大鼠胸主动脉VSMCs，Western blot检测p-ERK1／2、ERK1／2、细胞周期蛋白CyclinDl和CyclinE的表达，四噻唑蓝比色法观察PKC阻断剂GF109203X对apelin-13促大鼠VSMCs增殖的影响。结果Apelin-13剂量依赖性和时间依赖性地促进大鼠VSMCsp-ERK1／2表达增加，对ERK1／2表达没有明显影响，GF109203X可明显抑制apelin-13诱导的细胞增殖及p-ERK1／2、CyclinDl和CyclinE的表达。结论Apelin-13促进大鼠VSMCs增殖可能与apelin—APJ—PKC—ERK1／2-Cyclins信号通路有关。
摘要：
AIM: To investigate the mechanism by which probucol (PBC) affected adhesion of monocytes to human umbilical vein endothelial cells (HUVEC). METHODS: Effects of PBC on expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, a nd E-selectin in human umbilical vein endothelial cells were examined. Moreover, the inhibitory effect of PBC were compared with that of monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, P-selectin, and E-select in on adhesion induced by oxidized-low density lipoprotein(Ox-LDL). RESULTS: PBC at 10 to 80 micromol/L inhibited Ox-LD L-induced adhesion index from 16.7 % to 7.0 % (P < 0.01) and Ox-LDL-induced expression of ICAM-1 (75 %) and P-selectin (72 %). mAbs to ICAM -1 or P-selectin, when used alone, could only slightly reduce the adhesion of monocyte to HUVEC. When both monoclonal antibodies were used in combination, the adhesion was markedly inhibited from 16.7 % to 11.3 % (P < 0.01), but the effect was still weaker than that of PBC (average 9.3 %). CONCLUSION: PBC exerts its inhibitory effect on the adhesion of monocyte to HUVEC by inhibiting the expression of ICAM-1 and P-selectin.
摘要：
AIM: To investigate the mechanism by which probucol (PBC) affected adhesion of monocytes to human umbilical vein endothelial cells (HUVEC). METHODS: Effects of PBC on expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, and E-selectin in human umbilical vein endothelial cells were examined. Moreover, the inhibitory effect of PBC were compared with that of monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, P-selectin, and E-selectin on adhesion induced by oxidized-low density lipoprotein (Ox-LDL). RESULTS: PBC at 10 to 80 μmol/L inhibited Ox-LDL induced adhesion index from 16.7 % to 7.0 % (P < 0.01) and Ox-LDL-induced expression of ICAM-1 (75 %) and P-selectin (72 %). mAbs to ICAM-1 or P-selectin, when used alone, could only slightly reduce the adhesion of monocyte to HUVEC. When both monoclonal antibodies were used in combination, the adhesion was markedly inhibited from 16.7 % to 11.3 % (P < 0.01), but the effect was still weaker than that of PBC (average 9.3 %). CONCLUSION: PBC exerts its inhibitory effect on the adhesion of monocyte to HUVEC by inhibiting the expression of ICAM-1 and P-selectin.
作者机构：
[Chen, WZ] Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China.;Hengyang Med Coll, Dept Pharmacol, Hengyang 421001, Peoples R China.
通讯机构：
[Chen, WZ] C;Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China.
关键词：
Eposprostenol;Flavones;Ginggolides;Ginkgo biloba;Lysophosphatidylcholines;Malondialdehyde;Thoracic aorta;Vascular endothelium;Vitamin E
摘要：
AIM: To study the protective effects of Ginkgo biloba extract (GbE) against endothelial cell damage induced by lysophosphatidylcholine (LPC). METHODS: The vasorelaxation response to acetylcholine (ACh) were investigated in the isolated rabbit thoracic aorta. Lipid peroxidation products were determined by measuring thiobarbituric acid reactive substance. RESULTS: GbE attenuated the inhibition of vasorelaxation response to ACh and prevented the LPC-induced increase of malondialdehyde (MDA) content both in thoracic aortae. GbE prevented the leakage of LDH and the increase of MDA content in cultured endothelial cells in a concentration-dependent manner. GbE also markedly increased epoprostenol level in cultured endothelial cells treated with LPC. CONCLUSION: GbE protected endothelial cells against LPC-induced damage due to reduction in lipid peroxidation and facilitation of synthesis and/or release of eposprostenol.
