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Protective effects of baicalein against rotenone-induced neurotoxicity in PC12 cells and isolated rat brain mitochondria
Baicalein is one of the major flavonoids obtained from the Scutellaria root. Previous pharmacological studies found that baicalein had neuroprotective effects in animal models of Parkinson's disease. The purpose of this paper was to explore the molecular mechanism of the action of baicalein on PC12 cells and isolated rat brain mitochondria. Firstly, we investigated the effects of baicalein on rotenone-induced toxicity in PC12 cells. The results showed that baicalein suppressed rotenone-induced apoptosis, and inhibited the accumulation of reactive oxidant species, ATP deficiency, mitochondrial membrane potential dissipation, and caspase-3/7 activation in a concentration-dependent manner, indicating that baicalein likely improved mitochondrial function. Furthermore, we used isolated rat brain mitochondria to evaluate the effect of baicalein. Treatment with baicalein prevented rotenone-induced reactive oxidant species production, ATP deficiency and mitochondrial swelling in isolated brain mitochondria. Interestingly, exposure of isolated mitochondria to baicalein promoted mitochondrial active respiration. These results suggest that baicalein may be a mitochondria-targeted antioxidant and exerts neuroprotective effects on rotenone-induced neurotoxicity. This study supports our previous research that baicalein possesses neuroprotective activity in vivo and it is worthy of further study.
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Tissue accumulation of homocysteine occurs in classical homocystinuria, a metabolic disease characterized biochemically by cystathionine β-synthase deficiency. Vascular manifestations such as myocardial infarction, cerebral thrombosis, hepatic steatosis, and pulmonary embolism are common in this disease and poorly understood. In this study, we investigated the effect of chronic hyperhomocysteinemia on some parameters of oxidative stress (thiobarbituric acid-reactive substances, protein carbonyl content, 2′,7′-dichlorofluorescein fluorescence assay, and total radical-trapping antioxidant potent) and activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) in the rat lung. Reduced glutathione content and glucose 6-phosphate dehydrogenase activity, as well as nitrite levels, were also evaluated. Wistar rats received daily subcutaneous injections of Hcy (0.3–0.6 μmol/g body weight) from the 6th to the 28th days-of-age and the control group received saline. One and 12 h after the last injection, rats were killed and the lungs collected. Hyperhomocysteinemia increased lipid peroxidation and oxidative damage to protein, and disrupted antioxidant defenses (enzymatic and non-enzymatic) in the lung of rats, characterizing a reliable oxidative stress. In contrast, this amino acid did not alter nitrite levels. Our findings showed a consistent profile of oxidative stress in the lung of rats, elicited by homocysteine, which could explain, at least in part, the mechanisms involved in the lung damage that is present in some homocystinuric patients.
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Chronic kidney disease (CKD) is associated with accelerated atherosclerosis and increased mortality from cardiovascular disease. CKD results in oxidative stress, inflammation, and high-density lipoprotein (HDL) deficiency, which work in concert to promote atherosclerosis. Normal HDL confers protection against atherosclerosis by inhibiting the oxidation of lipids and lipoproteins and by retrieving surplus cholesterol and phospholipids from lipid-laden cells in the artery wall for disposal in the liver (reverse cholesterol transport).
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