Diabetes Mellitus Alters the Immuno-Expression of Neuronal Nitric Oxide Synthase in the Rat Pancreas.
Bright Starling EmeraldSahar MohsinCrystal D'SouzaAnnie JohnHussain El-HasasnaShreesh Kumar OjhaHaider RazaBasel Al-RamadiErnest A AdeghatePublished in: International journal of molecular sciences (2022)
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.
Keyphrases
- nitric oxide synthase
- nitric oxide
- glycemic control
- type diabetes
- hydrogen peroxide
- cardiovascular disease
- induced apoptosis
- diabetic rats
- poor prognosis
- magnetic resonance
- oxidative stress
- weight loss
- stem cells
- cell cycle arrest
- randomized controlled trial
- wound healing
- clinical trial
- cell proliferation
- mesenchymal stem cells
- spinal cord
- subarachnoid hemorrhage
- skeletal muscle
- brain injury
- endoplasmic reticulum stress
- pi k akt