Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson’s Disease

Abstract

ing potentiation of lipid peroxidation, reduction in the concentrations of reduced glutathione and antioxidant enzyme activity, increased malondialdehyde concentration, and disruption of iron metabolism. Environmental toxins and genetic disorders associated with apoptosis and protein breakdown may also play a role [2,3]. Oxidative stress leads to the damage of extremely sensitive neurons and is an important factor in both the initiation and progression of PD. This damage is revealed by increases in either the oxidation or reduction activity of enzymes with antioxidant activity. These changes to the oxidation-antioxidant system may also simultaneously affect both oxidation and reduction Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder affecting 1% of the population over the age of 55, and the risk of PD is significantly increased in the elderly [1]. As PD progresses, dopaminergic neurons in the substantia nigra of the midbrain are lost as a result of the progressive degenerative process revealed by a reduction in dopamine levels in this structure [2]. Despite years of research, the pathogenesis of PD is not fully understood, although many factors are thought to be involved. One hypothesis is that PD is caused by increased oxidative stress. Roles for the oxidation-oxidant system in other disorders have been confirmed by numerous studies demonstrat- Objectives. The present study aimed to evaluate selected parameters of the liver oxidative-antioxidative system in a Wistar rat model with Parkinson's disease treated with propofol. Material and Methods. Experiments were performed on 32 rats divided into 4 groups: 1 -control, 2 -Parkinson's disease, 3 -control with propofol, 4 -Parkinson's disease with propofol. The rats were decapitated at 8 weeks of age and their livers were collected. In the liver, the activities of catalase (CAT), glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR) and the concentrations of: Malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS) were assessed. Results. The study demonstrated a decrease in CAT activity and an increase in MDA, TOS concentrations in group 2 compared to that of group 1. Administration of propofol in rats of group 4 caused an increase in CAT activity and a decrease in MDA concentration compared to that of group 2 and an increase in TAC, CAT, GR levels, decrease in MDA levels compared to that of group 1. There was also an increase in GR and TAC in group 3 compared to that of group 1. Conclusions. Propofol in Parkinson's disease stimulates the production of antioxidant enzymes in the liver, simultaneously decreasing oxidative stress, which has a beneficial effect on the oxidative-antioxidative balance (Adv Clin Exp Med 2016, 25, 5, 815-820).

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

“…The rat models of Parkinson’s disease were constructed in accordance with the research of Romuk et al [2], and the behavior test was conducted 8 weeks after 6-OHDA injection.…”

“…PD affects approximately 1% of the population aged 55 years and older; a positive correlation was found between the risk of PD and age [2]. PD is characterized by motor symptoms including postural disturbance, akinesia, tremor, rigidity, and hypokinesia as well as non-motor symptoms including sleep disturbance, pain, apathy, depression, and constipation [1].…”

“…Several cellular abnormalities underlying neurodegeneration are present in sporadic PD, including oxidative stress (OS), proteasomal stress, mitochondrial dysfunction, and excitotoxicity, which are also involved in mutations of some familial PD genes [3]. Although multiple risk factors are involved in the occurrence and progression of PD, the pathogenesis remains unclear [2]. However, in many PD cases, OS seems to be a common potential mechanism that gives rise to cell dysfunction and death [4].…”

MicroRNA‐326 suppresses iNOS expression and promotes autophagy of dopaminergic neurons through the JNK signaling by targeting XBP1 in a mouse model of Parkinson's disease

“…Inducible nitric oxide synthase (iNOS) is also reported to be linked to neuroinflammatory responses operative in PD and other neurodegenerative disorders . Although multiple risk factors, such as environmental factors, genetic susceptibility, and aging, are involved in the occurrence and progression of PD, the pathogenesis still remains unclear . Thus this calls for newer and more accurate predictors to help provide better diagnosis and prognosis of PD.…”

Effect of propofol on the skeletal muscle insulin receptor in rats with hepatic ischemia-reperfusion injury

“…20,21 As a commonly used intravenous anesthetic, propofol has a strong antioxidant capacity, and may improve the antioxidant capacity of red blood cells and tissues in rats. 22,23 Our study demonstrated that tyrosine phosphorylation levels of Tyr-IRb and Tyr-IRS1 in the P group were higher than those the I/R group, indicating that an improvement in insulin signaling may result in reduced hyperglycemia.…”