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目的：探讨Nesfatin-1 对卡巴胆碱诱导的离体大鼠胃粘膜细胞胃酸分泌的影响及其机制。方法：采用酶解法分离原代SD 大鼠胃粘膜细胞。Nesfatin-1(10-1 umol/L)作用大鼠胃粘膜细胞不同时间以及不同浓度Nesfatin-1(10-1、10-2、10-3、10-4 umol/L)作用大鼠胃粘膜细胞0.5 h后，通过14C-氨基比林(14C-Aminopyrine，14C-AP)法检测其对卡巴胆碱(100 umol/L)诱导的大鼠胃粘膜细胞胃酸分泌的影响。将Nesfatin-1(10-1 umol/L)与卡巴胆碱(100 umol/L)共孵育大鼠胃粘膜细胞0.5 h 后，通过透射电镜观察胃壁细胞超微结构的变化。结果：Nesfatin-1(10-1 umol/L)作用于大鼠胃粘膜细胞0.5 h、1.0 h及10-1、10-2、10-3 umol/L Nesfatin-1 作用于大鼠胃粘膜细胞0.5 h 均可明显降低卡巴胆碱诱导的14C-AP 摄取量，与卡巴胆碱组相比，差异有统计学意义(P<0.05)；Nesfatin-1 可影响卡巴胆碱诱导的大鼠胃壁细胞的超微结构，抑制其从静息态向分泌态转化。结论：Nesfatin-1 可能通过影响胃壁细胞超微结构变化抑制卡巴胆碱诱导的SD 大鼠胃粘膜细胞的胃酸分泌。

英文摘要:

Objective:To investigate the effects and mechanisms of Nesfatin-1 on carbachol-stimulated gastric acid secretion in isolated rat gastric mucosal cells.Methods:Gastric mucosal cells of SD rats were isolated by enzymatically dispersion and treated by Nesfatin-1 (10-1滋mol/L) for different time or Nesfatin-1 (10-1, 10-2, 10-3, 10-4 滋mol/L) for 0.5 h. Then 14C-Aminopyrine (14C-AP) accumulation was gauged as a measure of acid secretion to detect Nesfatin-1 on carbachol-induced gastric acid secretion in isolated rat gastric mucosal cells. Subsequently, the rat gastric mucosal cells were coincubated with Nesfatin-1 (10-1umol/L) and carbachol (100 umol/L) for 0.5 h, transmission electron microscopywas used to observe the changes of parietal cells ultrastructure.Results:The carbachol-induced 14C-AP accumulation in isolated rat gastric mucosal cells were significantly inhibited by Nesfatin-1 (10-1 umol/L) for 0.5 h and 1 h or Nesfatin-1(10-1, 10-2, 10-3 umol/L) for 0.5 h(P<0.05). Electronic microscope results showed that parietal cells transformed from resting to stimulated states in response to extracellular stimulation by carbachol (100 umol/L), which was inhibited by Nesfatin-1 (10-1 umol/L).Conclusion:Nesfatin-1 could inhibit carbachol-induced gastric acid secretion in isolated rat gastric mucosal cells at least partly through influencing the ultrastructure of parietal cells.

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