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糖尿病改变大鼠胰腺神经元型一氧化氮合酶的免疫表达。

Diabetes Mellitus Alters the Immuno-Expression of Neuronal Nitric Oxide Synthase in the Rat Pancreas.

机构信息

Departments of Anatomy, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain P.O. Box 17666, United Arab Emirates.

Departments of Biochemistry, College of Medicine & Health Sciences, United Arab Emirates University, Al Ain P.O. Box 17666, United Arab Emirates.

出版信息

Int J Mol Sci. 2022 Apr 29;23(9):4974. doi: 10.3390/ijms23094974.

Abstract

Nitric oxide is generated from nitric oxide synthase following hyperglycemia-induced oxidative stress during the course of diabetes mellitus (DM). We examined the temporal immuno-expression of neuronal nitric oxide synthase (nNOS) in the pancreas of diabetic and non-diabetic rats using immunohistochemical, immunofluorescence and western blot techniques 12 h, 24 h, 1 week, 2 weeks, 1, 8 and 15 months after induction of DM. nNOS co-localized with pancreatic beta cells but disappears 12 h after the onset of DM. In contrast, the nNOS content of pancreatic nerves increased significantly (p < 0.001) 24 h after the induction of DM, and decreased sharply thereafter. However, nNOS-positive ganglion cells were observed even 15 months post-diabetes. ROS increased by more than 100% two months after the onset of DM compared to non-diabetic control but was significantly (p < 0.000001) reduced at 9 months after the induction of DM. The pancreatic content of GSH increased significantly (p < 0.02) after 9 months of DM. Although, TBARS content was significantly (p < 0.009; p < 0.002) lower in aged (9 months) non-diabetic and DM rats, TBARS rate was markedly (p < 0.02) higher 9 months after the induction of DM when compared to younger age group. In conclusion, nNOS is present in pancreatic beta cell, but disappears 12 h after the onset of diabetes. In contrast, the tissue level of nNOS of pancreatic nerves increased in the first week of diabetes, followed by a sharp reduction. nNOS may play important roles in the metabolism of pancreatic beta cell.

摘要

一氧化氮是在糖尿病(DM)过程中高血糖引起的氧化应激后,由一氧化氮合酶产生的。我们使用免疫组织化学、免疫荧光和 Western blot 技术,在糖尿病诱导后 12 h、24 h、1 周、2 周、1、8 和 15 个月,检查了糖尿病和非糖尿病大鼠胰腺中神经元型一氧化氮合酶(nNOS)的时间免疫表达。nNOS 与胰腺β细胞共定位,但在 DM 发病后 12 h 消失。相比之下,nNOS 含量的胰腺神经显著增加(p < 0.001)24 h 后,诱导 DM,此后急剧下降。然而,nNOS 阳性神经节细胞甚至在糖尿病后 15 个月仍被观察到。ROS 比非糖尿病对照组高出 100%以上,在 DM 发病后两个月,但在 DM 诱导后 9 个月时显著降低(p < 0.000001)。GSH 的胰腺含量在 DM 后 9 个月显著增加(p < 0.02)。尽管 TBARS 含量在老年(9 个月)非糖尿病和糖尿病大鼠中显著降低(p < 0.009;p < 0.002),但在 DM 诱导后 9 个月时,TBARS 率明显升高(p < 0.02)与年轻组相比。总之,nNOS 存在于胰腺β细胞中,但在糖尿病发病后 12 h 消失。相比之下,糖尿病的第一周,胰腺神经的组织水平 nNOS 增加,随后急剧减少。nNOS 可能在胰腺β细胞的代谢中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94fd/9105024/880d1a6230d5/ijms-23-04974-g001.jpg

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