The aim of our study was to investigate the protective effects and underlying mechanisms of myricetin, a bioactive food compound, on brain injury and neurological deficits after ischemic stroke. Treatment of myricetin significantly attenuated oxygen-glucose deprivation (OGD)-induced cell death in SHSY5Y cells in vitro. In a rat model of cerebral ischemia, myricetin was administered intragastrically at 2 h before and every day after middle cerebral artery occlusion (MCAO). The effects of myricetin were evaluated by various biochemical assays and neurobehavioral tests. Treatment with myricetin resulted in decreased infarction volume, reduced neuronal loss as well as lessened production of reactive oxygen species (ROS) and malondialdehyde following MCAO. We also found evidence that myricetin treatment could enhance the activity of antioxidant enzymes and mitochondrial function. Meanwhile, myricetin treatment reversed the suppression of Nrf2 nuclear translocation, and increased HO-1 expression in the ipsilateral ischemic brain and in the normal brain. Moreover, our results suggested that myricetin treatment resulted in significant improvement in neurological function. In conclusion, treatment with myricetin attenuates brain injury and neurological deficits in a rat model of cerebral ischemia via improvement of mitochondrial function and activation of the Nrf2 pathway.
Atopic dermatitis (AD) is a common chronic inflammatory skin disease, characterized by a T helper (Th)-2 cell-dominant inflammatory infiltrate and a defective epidermal permeability barrier. 1,2 Itch (or pruritus) is the major symptom of AD and causes a negative impact on quality of life. Intense itching is an unpleasant sensation, which evokes a strong desire to scratch. Moreover, itch-induced scratching aggravates skin lesions, and a vicious itch-scratch circle and consequent skin barrier destruction are easily established. 3,4 Previous studies exhibited that reducing physical stimulus to the skin, such as nail clipping, inhibits the development of AD in patients and AD-like phenotypes in a spontaneous mouse model. 5,6 However, the underlying mechanism through which scratching exacerbates dermatitis remains to be investigated.Transient receptor potential vanilloid type 1 (TRPV1), a nonselective cation channel with high permeability to calcium widely expressed in the epidermal keratinocytes, can be activated by heat, capsaicin, mechanical stimulus and endogenous inflammatory mediators. Stimulation of TRPV1 is reported to trigger neurogenic inflammatory mediator and neuropeptide releases, which ultimately contributes to the development of pruritus and diverse dermatoses. 7,8 Given the involvement of the TRPV1 receptor in the itching associated with pruritic inflammatory skin disease, we hypothesized
The effect of amifostine plus CF was greater than amifostine or CF alone in preventing high-dose methotrexate-induced intestinal mucositis and improving intestinal recovery in mice.
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