Background: Manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme that scavenges superoxide radicals found in the mitochondria, has been shown to protect oxygen-utilizing cells from the toxicity of the reactive oxygen species (ROS). Current studies in the animal esophageal reflux model are limited, and the reports on the relevance of protein expression level and enzymatic antioxidative activity of MnSOD in esophageal mucosal defense are controversial. Thus, the aim of this study is to investigate the role of MnSOD expression and activity in rats with esophageal perfusion injury.
Methods: We have established a novel external esophageal perfusion (EEP) animal model that allows for esophageal reflux injury. We used the model with 0.5% bovine bile as the perfusion agent in one group of rats and used saline in another group to serve as controls. The esophageal mucosal was isolated for MnSOD expression and activity analysis.
Results: Severe esophagitis was observed in the mucosa at 1, 2, and 4 week(s) after bile perfusion. A significant decrease in MnSOD expression with bile perfusion was demonstrated by Western blotting and immunohistochemical evaluation. Similarly, a reduction in MnSOD enzyme activity was observed in bile-perfused rats compared with the saline-perfused controls; no decrease in copper/zinc SOD enzyme activity was observed.
Conclusions: MnSOD expression and activity is decreased in bile-induced esophagitis. This decrease in MnSOD expression and activity is associated with esophagitis and cell death. This study suggests that the loss of MnSOD protein contributes to the reduced level of its enzymatic activity and plays a key role in the induction of esophagitis.
Background: The most prevalent endocrine disorder affecting women is PCOS. Programmed death of ovarian cells has yet to be elucidated. Ferroptosis is a kind of iron-dependent necrosis featured by significantly Fe-dependent lipid peroxidation.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
Background: Inclusion body myositis (IBM) is the most prevalent muscle disease in adults for which no current treatment exists. The pathogenesis of IBM remains poorly defined. In this study, we aimed to explore the interplay between inflammation and mitochondrial dysfunction in IBM.
Background: Women who had preeclampsia (a history of preeclampsia) have a >4-fold risk of developing cardiovascular disease compared with women who had an uncomplicated pregnancy (history of healthy pregnancy). Despite the remission of clinical symptoms after pregnancy, vascular endothelial dysfunction persists postpartum, mediated in part by exaggerated Ang II (angiotensin II)-mediated constriction. However, the role of vasodilatory ATRs (Ang II type 2 receptors) in this dysfunction is unknown.
Objectives: To explore the effect and the probable mechanisms of JLD in the treatment of type 2 diabetes mellitus (T2DM) - associated cognitive impairment (TDACI).
Methods: The effect of JLD in combating TDACI was assessed in T2DM model mice by conducting Morris water maze (MWM) behaviour testing. Active components and their putative targets, as well as TDACI-related targets, were collected from public databases.
