The hepato-protective effect of H2S-modified and non-modified mesenchymal stem cell exosomes on liver ischemia-reperfusion injury in mice: The role of MALAT1.

Introduction: Ischemia-reperfusion injury (IRI) by causing histopathological changes is considered one of the most important causes of liver failure and dysfunction after surgery which affect graft outcomes. Stem cells are new promising approaches to treating different diseases. One of the critical strategies to improve their function is the preconditioning of their culture medium.

Characterization of diet based nonalcoholic fatty liver disease/nonalcoholic steatohepatitis in rodent models: Histological and biochemical outcomes.

Nonalcoholic fatty liver disease (NAFLD), as the most common chronic liver disease, is rapidly increasing worldwide. This complex disorder can include simple liver steatosis to more serious stages of nonalcoholic fibrosis and steatohepatitis (NASH). One of the critical concerns in NASH research is selecting and confiding in relying on preclinical animal models and experimental methods that can accurately reflect the situation in human NASH.

Neuroprotective effects of oral gallic acid against oxidative stress induced by 6-hydroxydopamine in rats.

Free radical-induced neural damage is implicated in neurodegenerative diseases and antioxidants have protective activity. In the present study, we examined the effect of gallic acid (GA; 50, 100 and 200mg/kg, p.o.

Motor disorders and impaired electrical power of pallidal EEG improved by gallic acid in animal model of Parkinson's disease.

The aim of this study was evaluation the effect of Gallic acid on movement disorders and pallidal electrical power in animal model of Parkinson's Disease (PD). PD is clinically characterized by development of motor disturbances, such as bradykinesia, resting tremors, rigidity and a later loss ofpostural reflexes. Oxidative stress is a hallmark factor where the oxidation of dopamine generates Reactive Oxygen Species (ROS) and an unbalanced production ROS induces neuronal damage, therefor leading the neuronal death.