These findings suggest the antidementia activity of caffeic acid against AlCl3 -induced dementia in rats. The outcome of present study offers a wider scope to screen caffeic acid against neurodegeneration associated disorders.

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: Benzothiazole is an organic compound bearing a heterocyclic nucleus (thiazole) which imparts a broad spectrum of biological activities to it. The significant and potent activity of benzothiazole moiety influenced distinctively by nature and position of substitutions. This review summarizes the effect of various substituents in recent trends and approaches to design and develop novel benzothiazole derivatives for anticancer potential in different cell lines by interpreting the Structure- Activity Relationship (SAR) and mechanism of action of a wide range of derivatives. The list of derivatives is categorized into different groups and reviewed for their anticancer activity. The structure-activity relationship for the various derivatives revealed an excellent understanding of benzothiazole moiety in the field of cancer therapy against different cancer cell line. Data obtained from the various articles showed the potential effect of benzothiazole moiety and its derivatives to produce the peculiar and significant lead compound. The important anticancer mechanisms found are tyrosine kinase inhibition, topoisomerase inhibition and induction of apoptosis by Reactive Oxygen Species (ROS) activation. Therefore, the design and development of novel benzothiazole have broad scope in cancer chemotherapy.

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Insulin is a cytokine which promotes cell growth. Recently, a few published reports on insulin in different cell lines support the antiapoptotic effect of insulin. But the reports fail to explain the role of insulin in modulating glutamate-mediated neuronal cell death through excitotoxicity. Thus, we examined the neuroprotective effect of insulin on glutamate-induced toxicity on differentiated SH-SY5Y neuronal cells. Changes in cell viability were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) based assay, while apoptotic damage was detected by acridine orange/ethidium bromide and Hoechst staining. Intracellular reactive oxygen species (ROS) accumulation and morphological alterations were also measured. Treatment with glutamate induced apoptosis, elevated ROS levels and caused damage to neurons. Insulin was able to attenuate the glutamate-induced excitotoxic damage to neuronal cells.

Objectives. Aluminium, a neurotoxic agent in humans, has been implicated in the pathogenesis of neurodegenerative disorders. In this study, we examined the behavioral and biochemical effects of aluminium in rats with special emphasis on memory centres, namely, hippocampus and frontal cortex. Further, the effect of simvastatin treatment on aluminium intoxication was evaluated. Methods. Rats were exposed to aluminium chloride (AlCl3) for 60 days. Simvastatin (10 mg/kg/p.o.) and rivastigmine (1 mg/kg/p.o.) were administered daily prior to AlCl3. Behavioral parameters were assessed using Morris water maze test and actophotometer followed by biochemical investigations, namely, acetylcholinesterase (AChE) activity, TNF-α level, antioxidant enzymes (GSH, catalase), lipid peroxidation, and nitrite level in hippocampus and frontal cortex. Triglycerides, total cholesterol, LDL, and HDL levels in serum were also determined. Key Findings. Simvastatin treatment improved cognitive function and locomotor activity in rats. Simvastatin reversed hyperlipidemia and significantly rectified the deleterious effect of AlCl3 on AChE activity. Further, in hippocampus and frontal cortex, aluminium-induced elevation in nitrite and TNF-α and reduction in antioxidant enzymes were inhibited by simvastatin. Conclusion. To conclude, the present study suggests that simvastatin per se protects the neurons in hippocampus and frontal cortex from AlCl3, an environmental toxin.

Catechin is an active ingredient of green tea. It is reported to inhibit corticosteroid-induced anxiety and depression-like symptoms. Considering the complex nature of depression, effects of catechin need to be studied in a clinically relevant depression model. The present study was designed to explore the antidepressant effect of catechin in Sprague Dawley rats subjected to chronic unpredictable mild stress (CUMS). Animals were subjected to CUMS and treated with (+)-catechin (50 mg/kg) or escitalopram (10 mg/kg) orally; a CUMS control and a vehicle control that was not exposed to CUMS were also established. Various stressors were applied daily in an unpredictable manner for 8 weeks achieve CUMS. Sucrose preference test were performed after 4 and 8 weeks and forced swim tests (FSTs) were conducted at weeks 4, 6 and 8. At the end of week 8, animals were sacrificed and the brain homogenate was studied for antioxidant parameters. Compared with the vehicle control, animals of the CUMS control group showed a significant decrease in sucrose intake. Catechin and escitalopram treatment significantly improved the sucrose intake compared with the CUMS control. A similar trend was observed in the FSTs, where catechin and escitalopram treatment significantly reduced the immobility time, and antioxidant parameters, including catalase, glutathione and superoxide dismutase levels were recovered in treated animals compared with the CUMS control. Thus, it was concluded that catechin reverses CUMS-induced depression in rats by ameliorating oxidative stress, which may help to develop a novel treatment for major depressive disorder.

Incorporating the phytosomal form of silymarin in liposomal carrier system increased the oral bioavailability and showed better hepatoprotection and better anti-inflammatory effects compared with silymarin suspension.