Cai Ying-Lan, Xu Dong-Yuan, Li Xiang-Lan, Qiu Zhang-Xun, Jin Zheng, Xu Wen-Xie
Department of Physiology, Yanbian University School of Medicine, 1829 Juzi Rd, Yanji 133000, Jilin Province, China.
World J Gastroenterol. 2009 May 7;15(17):2125-31. doi: 10.3748/wjg.15.2125.
To study the sensitivity of gastric smooth muscle to C-type natriuretic peptide (CNP) in streptozotocin (STZ)-induced diabetic rats.
The spontaneous contraction of a gastric smooth muscle strip was recorded by using physiological methods in rats. The expressions of CNP and natriuretic peptide receptor-B (NPR-B) in gastric tissue were examined by using immunohistochemistry techniques in the diabetic rat.
At 4 wk after injection of STZ and vehicle, the frequency of spontaneous contraction of gastric smooth muscle was significantly reduced in diabetic rats, and the frequency was decreased from 3.10 +/- 0.14 cycle/min in controls to 2.23 +/- 0.13 cycle/min (n = 8, P < 0.01). However, the amplitude of spontaneous contraction was not significant different from the normal rat. CNP significantly inhibited spontaneous contraction of gastric smooth muscle in normal and diabetic rats, but the inhibitory effect was significantly potentiated in the diabetic rats. The amplitudes of spontaneous contraction were suppressed by 75.15% +/- 0.71% and 58.92% +/- 1.32% while the frequencies were decreased by 53.33% +/- 2.03% and 26.95% +/- 2.82% in diabetic and normal rats, respectively (n = 8, P < 0.01). The expression of CNP in gastric tissue was not changed in diabetic rats, however the expression of NPR-B was significantly increased in diabetic rats, and the staining indexes of NPR-B were 30.67 +/- 1.59 and 17.63 +/- 1.49 in diabetic and normal rat, respectively (n = 8, P < 0.01).
The results suggest that CNP induced an inhibitory effect on spontaneous contraction of gastric smooth muscle, potentiated in diabetic rat via up-regulation of the natriuretic peptides-NPR-B-particulate guanylyl cyclase-cyclic GMP signal pathway.
研究链脲佐菌素（STZ）诱导的糖尿病大鼠胃平滑肌对C型利钠肽（CNP）的敏感性。
采用生理学方法记录大鼠胃平滑肌条的自发收缩。运用免疫组织化学技术检测糖尿病大鼠胃组织中CNP和利钠肽受体-B（NPR-B）的表达。
注射STZ和赋形剂4周后，糖尿病大鼠胃平滑肌的自发收缩频率显著降低，频率从对照组的3.10±0.14次/分钟降至2.23±0.13次/分钟（n = 8，P < 0.01）。然而，自发收缩幅度与正常大鼠无显著差异。CNP可显著抑制正常和糖尿病大鼠胃平滑肌的自发收缩，但在糖尿病大鼠中抑制作用明显增强。糖尿病大鼠和正常大鼠的自发收缩幅度分别被抑制75.15%±0.71%和58.92%±1.32%，频率分别降低53.33%±2.03%和26.95%±2.82%（n = 8，P < 0.01）。糖尿病大鼠胃组织中CNP的表达未发生变化，然而NPR-B的表达在糖尿病大鼠中显著增加，糖尿病大鼠和正常大鼠的NPR-B染色指数分别为30.67±1.59和17.63±1.49（n = 8，P < 0.01）。
结果表明，CNP对胃平滑肌的自发收缩具有抑制作用，在糖尿病大鼠中通过上调利钠肽-NPR-B-颗粒型鸟苷酸环化酶-环磷酸鸟苷信号通路而增强。
