Effect of recombinant human edostatin on peritoneal angiogenesis in uremic peritoneal dialysis rats / 中华肾脏病杂志

ABSTRACT

Objective To study the effect of recombinant human edostatin on peritoneal angiogenesis in uremic peritoneal dialysis(PD) rats. Methods Forty male SD rats were randomly divided into 5 groups normal control rats (group 1), renal failure without PD rats (group 2), rats dialyzed with 4.25% PD solution (group 3), rats dialyzed with 4.25% PD solution and received subcutaneous injection of recombinant human endostatin 10 mg/kg (group 4), rats dialyzed with 4.25% PD solution and received subcutaneous injection of recombinant human endostatin 40 mg/kg (group 5). Recombinant human endostatin was given every other day during peritoneal dialysis period, total 14 times. After regular PD for 28 days, tissue immunohistochemical staining and RT-PCR were used to detect the mRNA and protein expressions of VEGF and bFGF in peritoneal tissues of each group rats. Microvessel density (MVD) of peritoneum was detected and quantified with anti-CD34 immunohistochemical staining. Results The mRNA and protein of VEGF and bFGF were expressed in each group. Compared to group 1, the mRNA and protein expression of VEGF and bFGF were significantly up-regulated in group 2 and group 3 (all P＜0.05). Compared with group 3, the mRNA and protein expression of VEGF and bFGF were significantly downregulated in group 4 and group 5 (all P＜0.05). Compared with group 4, the mRNA and protein expression of VEGF and bFGF were significantly down-regulated in group 5 (all P＜0.05). The new microvascular vessels in group 1 showed little or none. Compared with group 1, MVD was significantly increased in group 2 and group 3 (P＜0.05). Compared with group 3, MVD was significantly decreased in group 4 and group 5 (all P＜0.05). Conclusions Recombinant human endostatin can effectively inhibit rat peritoneal neoangiogensis. Down-regulated expression of VEGF and bFGF in peritoneum may be one of the mechanisms of recombinant human endostatin inhibiting peritoneal angiogenesis.