AIM: To examine the participation of HSP90 in portal hypertensive rat mesentery in vitro.METHODS: Immunohistochemistry and Western-blot were used to examine the expression of HSP90 in mesenteric vasculature. HSP90 mRN...AIM: To examine the participation of HSP90 in portal hypertensive rat mesentery in vitro.METHODS: Immunohistochemistry and Western-blot were used to examine the expression of HSP90 in mesenteric vasculature. HSP90 mRNA was detected by RT-PCR, and the role of HSP90 in hyperdynamic circulation was examined by in vitro mesenteric perfusion studies.RESULTS: HSP90 was overexpressed in endothelium of mesentery vasculature in animals with experimental portal hypertension induced by partial portal vein ligation (PVL) compared with normal animals. Geldanamycin (GA), a special inhibitor of HsPg0 signaling, attenuated ACh-dependent vasodilation but did not affect vasodilation in response to sodium nitroprusside in normal rats. In PVL animals, the perfused mesentery was hyporesponsive to vasoconstrictor methoxamine. GA significantly potentiated methoxamineinduced vasoconstrictor after PVL.CONCLUSION: HsPg0 plays a key role in NO-dependent hyperdynamic circulation in portal hypertension and provides a novel method for future treatment of portal hypertension.展开更多
AIM: To verify the expressing efficiency and angiogenesiseffect after administration of expression vector encodingfor vascular endothelial growth factor D in normal andischemic rat liver.METHODS: Ten female S-D rats w...AIM: To verify the expressing efficiency and angiogenesiseffect after administration of expression vector encodingfor vascular endothelial growth factor D in normal andischemic rat liver.METHODS: Ten female S-D rats were administrated withliver tissue dot injection of naked PCHO/hVEGF-D, 50 μg/dot, three dots for each. The same amount of physiologicalsaline was used as control in the neighboring lobe. ForteenS-D rats, using inflow occlusion of left lateral lobe, were dividedinto two groups, seven rats in each group. One was ischemicplasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 μg. The other received the equal amountof natural saline injection and designed as control. Theexpressions of hVEGF-D in mRNA and protein levels wereidentified by in situ hybridyzation and immunohistochemistry,respectively. Endothelial cells were labeled by the factor VIIIimmunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated andcompared statistically 8 days after injection.RESULTS: A large amount of hVEGF-D in mRNA level wasfound in both normal and ischemic plasmid groups and butnone in their corresponding control groups. The protein ofhVEGF was also highly expressed in both normal and ischemicplasmid groups than in the controls. The mean number ofcapillaries under microscopy (×200) of the plasmid group andcontrol was 10.2±2.78 vs7.1±2.02 (P＜0.05), and those ofischemic plasmid group and ischemic control were 7.43+1.72vs 4.71± 1.11 with statistical difference (P＜0.05).CONCLUSION; The naked PCHO/hVEGF-D dot injection tonormal, ischemic rat liver can produce comparatively highexpression of hVEGF in both protein and mRNA levels, andprominently increase the number of new capillaries aroundhepatic sinuses. Therefore, it could be another ideal choicefor the treatment of ischemic liver diseases.展开更多
基金the National Natural Science Foundation of China,No.30170920
文摘AIM: To examine the participation of HSP90 in portal hypertensive rat mesentery in vitro.METHODS: Immunohistochemistry and Western-blot were used to examine the expression of HSP90 in mesenteric vasculature. HSP90 mRNA was detected by RT-PCR, and the role of HSP90 in hyperdynamic circulation was examined by in vitro mesenteric perfusion studies.RESULTS: HSP90 was overexpressed in endothelium of mesentery vasculature in animals with experimental portal hypertension induced by partial portal vein ligation (PVL) compared with normal animals. Geldanamycin (GA), a special inhibitor of HsPg0 signaling, attenuated ACh-dependent vasodilation but did not affect vasodilation in response to sodium nitroprusside in normal rats. In PVL animals, the perfused mesentery was hyporesponsive to vasoconstrictor methoxamine. GA significantly potentiated methoxamineinduced vasoconstrictor after PVL.CONCLUSION: HsPg0 plays a key role in NO-dependent hyperdynamic circulation in portal hypertension and provides a novel method for future treatment of portal hypertension.
基金the National Science Fund for Postdoctoral Fellows in China,No 2001.6the Medical Science Found of Shandong Province,No.2001CA1DBA10
文摘AIM: To verify the expressing efficiency and angiogenesiseffect after administration of expression vector encodingfor vascular endothelial growth factor D in normal andischemic rat liver.METHODS: Ten female S-D rats were administrated withliver tissue dot injection of naked PCHO/hVEGF-D, 50 μg/dot, three dots for each. The same amount of physiologicalsaline was used as control in the neighboring lobe. ForteenS-D rats, using inflow occlusion of left lateral lobe, were dividedinto two groups, seven rats in each group. One was ischemicplasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 μg. The other received the equal amountof natural saline injection and designed as control. Theexpressions of hVEGF-D in mRNA and protein levels wereidentified by in situ hybridyzation and immunohistochemistry,respectively. Endothelial cells were labeled by the factor VIIIimmunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated andcompared statistically 8 days after injection.RESULTS: A large amount of hVEGF-D in mRNA level wasfound in both normal and ischemic plasmid groups and butnone in their corresponding control groups. The protein ofhVEGF was also highly expressed in both normal and ischemicplasmid groups than in the controls. The mean number ofcapillaries under microscopy (×200) of the plasmid group andcontrol was 10.2±2.78 vs7.1±2.02 (P＜0.05), and those ofischemic plasmid group and ischemic control were 7.43+1.72vs 4.71± 1.11 with statistical difference (P＜0.05).CONCLUSION; The naked PCHO/hVEGF-D dot injection tonormal, ischemic rat liver can produce comparatively highexpression of hVEGF in both protein and mRNA levels, andprominently increase the number of new capillaries aroundhepatic sinuses. Therefore, it could be another ideal choicefor the treatment of ischemic liver diseases.
