This study aimed to investigate the effects of morin on cerebral damage and blood–brain barrier (BBB) integrity in a middle cerebral artery occlusion (MCAO) and reperfusion model. Wistar rats were exposed to MCAO for 2 h, followed by reperfusion. Thirty mg/kg of morin was administered via intraperitoneal injection at the different time points: before ischemia, during ischemia, and at reperfusion. The rats were divided into five groups, including sham, vehicle, and three groups of morin. Twenty-four hours after reperfusion, the rats were tested for neurological deficits, and the brains were harvested to assess brain damage. In addition, brains were harvested 72 h to determine BBB disruption. We found that morin significantly reduced reactive oxygen species production and lipid peroxidation. It also decreased inflammation via reducing the expression of Toll-like receptor 4, nuclear factor kappa-beta. Morin ameliorated cerebral damage and reduced apoptosis through decreasing the cerebral infarct size, including apoptotic cell death. Moreover, morin decreased the BBB damage via reducing Evans blue extravasation, neutrophil infiltration, and increasing tight junction protein expression. Therefore, morin protected against cerebral and BBB damage by attenuating oxidative stress, inflammation, and apoptosis in MCAO and reperfusion models.

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The demand for the production of herbal extracts for cosmetics, food, and health supplements, known as plant-based medicine, is rising globally. Incorporating herbal extracts could help to create higher value products due to the functional properties of bioactive compounds. Because the phytochemical composition could vary depending on the processing methods, a simple bioassay of herbal bioactive compounds is an important screening method for the purposes of functional characterization and quality assurance. As a simplified eukaryotic model, yeast serves as a versatile tool to examine functional property of bioactive compounds and to gain better understanding of fundamental cellular processes, because they share similarities with the processes in humans. In fact, aging is a well-conserved phenomenon between yeast and humans, making yeast a powerful genetic tool to examine functional properties of key compounds obtained from plant extracts. This study aimed to apply a well-established model yeast, Saccharomyces cerevisiae, to examine the antioxidant and anti-aging potential of flavonoids, extracted from medicinal plants, and to gain insight into yeast cell adaptation to oxidative stress. Some natural quercetin analogs, including morin, kaempferol, aromadendrin, and steppogenin, protected yeast cells against oxidative stress induced by acetic acid, as shown by decreased cell sensitivity. There was also a reduction in intracellular reactive oxygen species following acetic acid treatment. Using the chronological aging assay, quercetin, morin, and steppogenin could extend the lifespan of wild-type S. cerevisiae by 15%–25%. Consistent with the fact that oxidative stress is a key factor to aging, acetic acid resistance was associated with increased gene expression of TOR1, which encodes a key growth signaling kinase, and MSN2 and MSN4, which encode stress-responsive transcription factors. The addition of the antioxidant morin could counteract this increased expression, suggesting a possible modulatory role in cell signaling and the stress response of yeast. Therefore, yeast represents a versatile model organism and rapid screening tool to discover potentially rejuvenescent molecules with anti-aging and anti-oxidant potential from natural resources and to advance knowledge in the molecular study of stress and aging.

Stephania venosa (Blume) Spreng. is a medicinal herb wildly used as a folklore medicine in Thailand. Many studies have reported that S. venosa tuber revealed a variety of pharmacological activities including anti-malarial, anti-microbial, anti-cancer, anti-oxidant, and anti-inflammatory activities. In this study, we investigated the effects of (–)-stephanine and dehydrostephanine isolated from S. venosa tuber on anti-inflammation in lipopolysaccharide (LPS)-activated RAW264.7 macrophages. RAW264.7 cells were treated with (–)-stephanine and dehydrostephanine in the presence of LPS and cell viability was determined by MTT assay. The levels of inflammatory mediators, nitric oxide (NO) and pro-inflammatory cytokines were determined by Griess reagent and enzyme-linked immunosorbent assay, respectively. Pre-treatment of dehydrostephanine significantly suppressed NO secretion in LPS-activated RAW264.7 cells with the half-maximal NO inhibitory concentration (IC50) value of 26.81±0.25 μM. However, (–)-stephanine had IC50 value on the inhibition of NO secretion of >40 μM. In addition, dehydrostephanine at concentrations of 20 - 80 μM significantly reduced LPS-induced tumor necrosis factor-α, interleukin-1b, and interleukin-6 production in RAW264.7 cells. The present study showed that dehydrostephanine possesses the anti-inflammatory effect on LPS-activated RAW264.7 macrophages by suppression of inflammatory mediators. Dehydrostephanine may be a promising candidate compound for further investigation of a novel class of anti-inflammatory drug.