Mouse LPO(Lactoperoxidase) ELISA Kit

Parkinson disease occurs due to the depletion of dopaminergic neurons in brain resulting in decreased dopamine level and abnormal protein aggregation. Chrysin is a flavonoid which possesses pharmacological properties against various diseases like hypertension, diabetes, cancer, etc. According to the recent literatures, it is evidenced that chrysin protects mice against Focal Cerebral Ischemia/Reperfusion Injury. The present study aimed to elucidate the effect of chrysin on neuronal restoration in MPTP intoxicated acute mice model. From the results, it is revealed that the pre-treatment with chrysin protected MPTP induced degeneration of nigra-striatal neurons. It is observed that chrysin also ameliorates MPTP induced oxidative stress in mice by upregulating GSH, SOD and downregulating LPO levels. The motor dysfunction is also found to be enhanced which was evidenced through Beam walk, Horizontal grid and vertical grid tests. Pre-treatment with chrysin also averted MPTP induced alterations in neurotrophic factors, inflammatory markers and Dopamine contents. The findings of the present study clearly indicated that the chrysin reversed the neurochemical deficits, oxidative stress and behavioral abnormalities in PD mice and offers promising strategy for the treatment of neurodegenerative diseases.

We studied lipid peroxidation and measured the products of lipid peroxidation (LPO) together with the indices of the antioxidant system (AOS) in the blood of patients with epilepsy of various severities in the South Kazakhstan region of Kazakhstan. We examined 95 epileptic patients, including 35 patients with 3 seizure attacks per year, 30 patients with up to 12 seizure attacks per year, and 30 patients with more than 12 seizure attacks per year, that is, low, moderate, and severe levels of epilepsy, respectively, and 30 healthy men. We measured LPO products with simultaneous estimation of activity of superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPO) as well as antiradical (ARA) and antioxidant activity (AOA) in biological fluids. We also studied non-enzymatic antioxidant indices, such as the contents of alpha-tocopherol and SH-groups depending on epilepsy severity. We found that the content of LPO products in red blood cells and the deficit of the mechanisms of antioxidant defense increased depending on the severity of epilepsy in patients. In parallel to the increase in the level of lipid peroxides, lipid oxidizability was also enhanced in the blood of epileptic patients. Insufficiency of alpha-tocopherol was associated with decreased activity of SOD, AOA, and ARA in the body of patients. This complex study indicates that in epilepsy accumulation of lipid peroxides in the blood and a decrease in the activity of the AOS in the body occur. The expression of these processes directly depends on the severity of epilepsy.