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Introduction: Alzheimer’s disease (AD) is an age-dependent neurodegenerative disorder and major cause of mortality in the elderly. AD has a complex pathophysiology and needs new multi-targeted compounds to halt the disease progression through several mechanisms. Medicinal plants contain various compounds with heterogeneous pharmacological effects, therefore are a good source. The aim of this study was to evaluate the protective effect of total extracts of Sanguisorba minor and Ferulago angulata on beta-amyloid (Aβ)-induced toxicity in primary neural cell culture.Methods: Cerebellar granule neurons (CGNs) were cultured according to standard protocols. The cultured neurons were incubated with Aβ alone or in combination with different concentrations of extracts for 24 hours. Cell viability was measured by methylthiazolyldiphenyl-tetrazolium (MTT) assay. In addition acetylcholinesterase (AChE) activity and oxidative stress markers were measured after incubation. Also, the effects of different concentrations of the extracts on AChE activity of the cultured neurons were investigated. For measuring the acute toxicity of the extract, LD50 was estimated by limit test.Results: Both extracts could protect CGNs against Aβ-induced cell death. Aβ-induced oxidative stress and increase of AChE activity were ameliorated by both extracts. S. minor extract dose-dependently reduced AChE activity in cultured CGNs. LD50 of both extracts was estimated above 2000 mg/kg and considered as safe.Conclusion: Both studied extracts protected CGNs against Aβ-induced toxicity by ameliorating oxidative stress mechanism. According to these results, these extracts are recommended for further investigation in AD treatment.

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We are constantly encountering with low doses of chemicals in everyday life rather than toxic doses at a time. So, ongoing low-dose exposures of environmental chemicals commonly encountered are very likely to cause an adverse health effects. Perfluorooctanoic acid (PFOA) is frequently used for production of an array of consumer products and industrial processes. The present study evaluated the underlying mechanisms of PFOA-induced liver damage and also potential protection by taurine. Male Wistar rats were exposed to PFOA alone and in combination with taurine (25, 50, and 100 mg/kg/day) by gavage for 4 weeks. Liver function tests as well as histopathological examinations were studied. Also, oxidative stress markers, mitochondrial function, and nitric oxide (NO) production in liver tissues were measured. In addition, the expression of apoptosis-related genes (caspase-3, Bax, and Bcl-2), inflammation-associated genes (TNF-α, IL-6, NF-B), and c-Jun-N-terminal kinase (JNK) were evaluated. Taurine significantly reversed serum biochemical and histopathological alterations in the liver tissue following exposure to PFOA (10 mg/kg/day). Similarly, taurine alleviated mitochondrial oxidative damage-induced by PFOA in the liver tissue. An increased Bcl2: Bax ratio with decrees in the expression level of caspase-3, and decreased expression of inflammatory markers (TNF-α and IL-6), NF-B, and JNK were also observed following the administration of taurine. These findings suggest a protective role of taurine against PFOA-induced hepatotoxicity via the inhibition of oxidative stress, inflammation, and apoptosis.