Introduction: In our earlier studies, we reported that rotenone-induced mitochondrial dysfunction, oxidative stress, and apoptosis in the brain of mice have been protected through treatment with Agaricus blazei (A. blazei) extract. The present study is focused on the efficacy of A. blazei in the mitigation of motor and nonmotor symptoms induced by rotenone. Materials and Methods: Mice were randomly divided into four groups and treated with rotenone and simultaneously with A. blazei. Results: Rotenone treatment altered both the motor and nonmotor behavioral deficits as compared to controls. Concurrent treatment with rotenone and A. blazei significantly restored these behavioral deficits. Conclusion: The results of the present study strengthen the fact that the nutritional supplement of A. blazei extract in rotenone-affected areas might offer the neuroprotection.

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Background: Reduced cerebral blood flow is associated with aging, neurodegenerative disorders, and an increased formation of reactive oxygen species. This study was designed to assess the potential use of vitamin E as an antioxidant and neuroprotective agent using 2-vessel occlusion (2VO) rat animal model. Materials and Methods: Twenty-four Sprague Dawley rats weighing 200–250 g were equally divided into the following three groups: SHAM control, 2VO, and 2VO+E (treated daily with vitamin E tocotrienol, 100 mg/kg, orally following 2VO). On the 8^th week after 2VO surgery, rats were euthanized and the hippocampi were isolated with the estimation of viable neuronal cell count in the hippocampal CA-1 region. The isoprostane F₂ (Iso-F2) levels were also measured in the brain homogenates to quantify the oxidative stress levels. Results: There was significantly higher neuronal cell death in the hippocampal CA-1 region and increased Iso-F2 levels in the 2VO group compared to the SHAM control group (P < 0.05). Conversely, no significant difference was observed with regard to the neuronal cell death and Iso-F2 levels in the 2VO+E group and the SHAM control group (P > 0.05). Conclusion: This study demonstrates the effectiveness of vitamin E tocotrienol as a neuroprotective and antioxidant agent in chronic cerebral hypoperfusion-induced neurodegeneration in rats.

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Introduction: Parkinson’s disease (PD) is a progressive age-related disease, in which dopaminergic neurons in the nigrostriatal pathway are destroyed, resulting in movement and behavioral impairment. Oxidative stress and the generation of reactive oxygen species play a key role in the progression and pathology of neurodegenerative diseases such as PD. Rotenone is a common pesticide that induces PD through the generation of oxidative stress. Isolongifolene (ILF), a tricyclic sesqueterpene of Murraya koenigii, has antioxidant and neuroprotective effects. The current study was aimed to investigate the effect of ILF against oxidative stress and movement impairment on rotenone-induced rat model of PD. Materials and Methods: Biochemical measures, including the activities of catalase, glutathione peroxidase (GPx), superoxide dismutase (SOD) and the levels of reduced glutathione (GSH) and lipid peroxidation products [thiobarbituric acid reactive substances (TBARS) and behavioral analysis (hang and catalepsy test) were performed. Results: The muscle strength and cataleptic score of the ILF co-treated groups were significantly improved. Treatment with ILF prevented the increases in the levels of TBARS, significantly improved the SOD, catalase, GPx activities, and GSH levels. Conclusion: These findings suggested that ILF has neuroprotective properties through its potent antioxidant activities.

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Introduction: In our earlier studies, we reported the neuroprotective effect of tannoid principles of Emblica officinalis (EoT) against aluminum chloride (AlCl₃)-induced neurotoxicity in the hippocampus and cortex of rats. The present study is focused on the efficacy of EoT in the mitigation of AlCl₃-induced toxicity in the cerebellum. Materials and Methods: Rats were randomly divided into four groups and treated with AlCl₃ (100 mg/kg, b.w. i.p.), EoT (100 mg/kg, b.w. oral), and simultaneously with AlCl₃ and EoT daily for 60 days. Results: AlCl₃ treatment altered the body weight, brain and cerebellum weight, Al levels, acetylcholinesterase activity, and the expression of apoptotic markers. Treatment with EoT attenuated these physiological, biochemical, and molecular indices. Conclusion: The results of the present study strengthen the fact that the nutritional supplement of EoT in AlCl₃-treated rats might improve the adverse effects by its pharmacological properties.

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Aim: To evaluate the effect of morin in ultraviolet-B (UV-B)-induced oxidative stress and inflammatory cytokines expression in the skin of Swiss albino mice. Materials and Methods: Swiss albino mice were divided into six treatment groups, and each group consisted of eight mice based on their exposure to UV-B radiation (180 mJ/cm²) and their respective treatment with morin (15 mg/kg). Morin was administered both intraperitoneally and topically thrice in a week for 30 weeks before UV-B exposure. After the treatment period, the mice were sacrificed, and the effect of morin on UV-B radiation-induced lipid peroxidation and enzymatic and nonenzymatic antioxidant levels was estimated on skin tissues spectrophotometrically. Western blot analysis was used to estimate the inflammatory cytokines. Results: This study revealed that the intraperitoneal and topical administration of morin significantly lowered the incidence of UV-B-induced tumor size in the skin of Swiss albino mice. Further, morin significantly reduced (P < 0.05) lipid peroxidation and increased the antioxidant levels in Swiss albino mice. It was also observed that morin reduced the expression of tumor necrosis factor-α and interleukin-6. Conclusion: Morin has a stimulative effect on endogenous antioxidant defense mechanisms. It can prevent the photo damage of macromolecules such as lipids and the oxidation of proteins, thereby reducing oxidative stress and inflammation.

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