Trans-anethole attenuates diet-induced nonalcoholic steatohepatitis through suppressing TGF-ß-mediated fibrosis.

BACKGROUND: Nonalcoholic Steatohepatitis (NASH) is the most severe type of non-alcoholic fatty liver disease (NAFLD) and one of the most common chronic liver diseases, leading to the increased risk of liver failure, cirrhosis and hepatocellular carcinoma. Trans-anethole was reported to have anti-inflammatory, anti-obesity and anti-diabetic activities. However, its role in NASH remains unknown. Therefore, we aimed to explore the effect of Trans-anethole on NASH. METHODS: Eight-week-old C57BL/6 mice were fed on a methionine- and choline-deficient (MCD) diet for 8 weeks to induce NASH in mice, and on the meanwhile, mice were also orally administrated with or without 100 mg/kg Trans-anethole daily to evaluate the effect of Trans-anethole on NASH. RESULTS: Trans-anethole dose-dependently ameliorated liver injury in MCD diet-fed mice, then the most effective dose of Trans-anethole 100 mg/kg was chosen. Trans-anethole significantly attenuated hepatic steatosis, inflammation and hepatic fibrosis in MCD diet-induced NASH mice. Moreover, Trans-anethole reduced hepatic fibrosis by inhibiting transforming growth factor-beta signaling pathway both in vivo and in vitro. CONCLUSION: Trans-anethole effectively ameliorated NASH in MCD diet-fed mice, which suggested that Trans-anethole might serve as a therapeutic strategy for NASH.

The Combination of ß-Asarone and Icariin Inhibits Amyloid-ß and Reverses Cognitive Deficits by Promoting Mitophagy in Models of Alzheimer's Disease.

ß-Asarone is the main constituent of Acorus tatarinowii Schott and exhibits important effects in diseases such as neurodegenerative and neurovascular diseases. Icariin (ICA) is a major active ingredient of Epimedium that has attracted increasing attention because of its unique pharmacological effects in degenerative disease. In this paper, we primarily explored the effects of the combination of ß-asarone and ICA in clearing noxious proteins and reversing cognitive deficits. The accumulation of damaged mitochondria and mitophagy are hallmarks of aging and age-related neurodegeneration, including Alzheimer's disease (AD). Here, we provide evidence that autophagy/mitophagy is impaired in the hippocampus of APP/PS1 mice and in Aß1-42-induced PC12 cell models. Enhanced mitophagic activity has been reported to promote Aß and tau clearance in in vitro and in vivo models. Meanwhile, there is growing evidence that treatment of AD should be preceded by intervention before the formation of pathological products. The efficacy of the combination therapy was better than that of the individual therapies applied separately. Then, we found that the combination therapy also inhibited cell and mitochondrial damage by inducing autophagy/mitophagy. These findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis, and that combination treatment with mitophagy inducers represents a potential strategy for therapeutic intervention.

Synthesis, antiepileptic effects, and structure-activity relationships of α-asarone derivatives: In vitro and in vivo neuroprotective effect of selected derivatives.

In the present study, we compared the antiepileptic effects of α-asarone derivatives to explore their structure-activity relationships using the PTZ-induced seizure model. Our research revealed that electron-donating methoxy groups in the 3,4,5-position on phenyl ring increased antiepileptic potency but the placement of other groups at different positions decreased activity. Besides, in allyl moiety, the optimal activity was reached with either an allyl or a 1-butenyl group in conjugation with the benzene ring. The compounds 5 and 19 exerted better neuroprotective effects against epilepsy in vitro (cell) and in vivo (mouse) models. This study provides valuable data for further exploration and application of these compounds as potential anti-seizure medicines.