Podvigina T T, Bagaeva T P, Filaretova L P
Ross Fiziol Zh Im I M Sechenova. 2016 Nov;102(11):1352-62.
The results of our previous studies suggest that corticotropin-releasing factor (CRF) protects the gastric mucosa of rats against stress- and indomethacin-induced gastric injury. In the present study, we investigated whether CRF may protect gastric mucosa against indomethacin-induced gastric injury on diabetic rats. Diabetes was induced by streptozotocin (70 mg/kg) 14 days before indomethacin injection. CRF (2.5 |xg/kg) and CRF receptor antagonists were injected 15 min before indomethacin. The diabetes development resulted in the aggravation of gastric mucosal erosion produced by indomethacin. Intraperitoneal CRF administration caused pronounced gastropro-tective action in control as well as diabetic rats that resulted in significant attenuation of indomethacin-induced gastric erosion. Nonselective antagonist CRF receptors astressin as well as selective antagonists of CRF1 and CRF2 receptors (NBI 27914, 10 mg/kg or astressin2-B, 50 |xg/kg, respectively) aggravated ulcerogenic effect of indomethacin in diabetic rats. The results obtained suggest that exogenous and endogenous CRF may protect the gastric mucosa of diabetic rats against indomethacin-induced injury through CRF1 and CRF2 receptors.
我们之前的研究结果表明，促肾上腺皮质激素释放因子（CRF）可保护大鼠胃黏膜免受应激和吲哚美辛诱导的胃损伤。在本研究中，我们调查了CRF是否可以保护糖尿病大鼠胃黏膜免受吲哚美辛诱导的胃损伤。在注射吲哚美辛前14天，用链脲佐菌素（70mg/kg）诱导糖尿病。在注射吲哚美辛前15分钟注射CRF（2.5μg/kg）和CRF受体拮抗剂。糖尿病的发展导致吲哚美辛引起的胃黏膜糜烂加重。腹腔注射CRF对对照组和糖尿病大鼠均产生显著的胃保护作用，导致吲哚美辛诱导的胃糜烂明显减轻。非选择性CRF受体拮抗剂阿斯特辛以及CRF1和CRF2受体的选择性拮抗剂（分别为NBI 27914，10mg/kg或阿斯特辛2-B，50μg/kg）加重了吲哚美辛对糖尿病大鼠的致溃疡作用。所得结果表明，外源性和内源性CRF可能通过CRF1和CRF2受体保护糖尿病大鼠胃黏膜免受吲哚美辛诱导的损伤。
