VASOACTIVE INTESTINAL PEPTIDE RECEPTORS IN BRAINS OF HEPATIC ENCEPHALOPATHY RATS AN EXPERIMENTAL STU

来源 :Chinese Medical Journal | 被引量 : 0次 | 上传用户:shenglove5
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We evaluated the effect of vasoactive intestinal peptide (VIP) receptor, a brain-gut peptide receptor which is capable of exciting central neurons, on the pathogenesis of hepatic encephalopathy (HE). By means of radio-ligand binding assay, VIP receptors in the crude synaptosomal membranes of rat brains were investigated in rat models with HE induced by partial hepatectomy following carbon tetrachloride intoxication and in controls. The binding to the VIP receptor was studied, with 125I-VIP as a radioligand. Scatchard analysis of the binding data was linear, yielding a dissociation constant (Kd) of 0.28 ± 0.01 nM and a maximal binding capacity (Bmax) of 9.56 ± 0.29 fmol / mg of protein in HE rats. Only decreased Bmax values were observed (P< 0.002), while the Kd values were statistically unchanged (P > 0.20) in HE rats as compared with the controls. The results suggest that the changes of VIP receptors in the brains of HE rats play a significant role in the pathogenesis of HE. The mechanism of HE induce We think the effect of vasoactive intestinal peptide (VIP) receptor, a brain-gut peptide receptor which is capable of exciting of central central neurons, on the pathogenesis of hepatic encephalopathy (HE). By means of radio-ligand binding assay, VIP receptors in the crude synaptosomal membranes of rat brains were investigated in rat models with HE induced by partial hepatectomy following carbon tetrachloride intoxication and in controls. The binding to the VIP receptor was studied, with 125I-VIP as a radioligand. Scatchard analysis of the binding data was linear , only decreased Bmax values ​​were observed (P <0.002), while the Kd values ​​(Kd) were 0.28 ± 0.01 nM and a maximal binding capacity (Bmax) of 9.56 ± 0.29 fmol / mg of protein in HE rats were statistically unchanged (P> 0.20) in HE rats as compared with the controls. The results suggest that the changes of VIP receptors in the brains of HE rats play a significant role in the pathogenesis of HE. The mec hanism of HE induce
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