Cannabidiol (CBD), an abundant nonpsychoactive constituent of marijuana, has been reported previously to protect against hepatic steatosis. In this study, we studied further the functions and mechanisms of CBD on liver inflammation induced by HFC diet. Mice feeding an HFC diet for 8 weeks were applied to test the protective effect of CBD on livers. RAW264.7 cells were incubated with LPS + ATP ± CBD to study the mechanisms of the effect of CBD against inflammasome activation. We found that CBD alleviated liver inflammation induced by HFC diet. CBD significantly inhibited the nuclear factor-κappa B (NF-κB) p65 nuclear translocation and the activation of nucleotide-binding domain like receptor protein 3 (NLRP3) inflammasome both in vivo and in vitro studies, which lead to the reduction of the expression of inflammation-related factors in our studies. In addition, Inhibitor of activation of NF-κB partly suppressed the NLRP3 inflammasome activation, while adding CBD further inhibited NF-κB activation and correspondingly suppressed the NLRP3 inflammasome activation in macrophages. In conclusion, the suppression of the activation of NLRP3 inflammasome through deactivation of NF-κB in macrophages by CBD might be one mechanism of its anti-inflammatory function in the liver. K E Y W O R D Scannabidiol, NF-κB, NLRP3 inflammasome, nonalcoholic steatohepatitis

Mounting evidence suggests that mitochondrial dysfunction and impaired mitophagy lead to Parkinson’s disease (PD). Quercetin, one of the most abundant polyphenolic flavonoids, displays many health-promoting biological effects in many diseases. We explored the neuroprotective effect of quercetin in vivo in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD and in vitro in 6-OHDA-treated PC12 cells. In vitro , we found that quercetin (20 μM) treatment improved mitochondrial quality control, reduced oxidative stress, increased the levels of the mitophagy markers PINK1 and Parkin and decreased α-synuclein protein expression in 6-OHDA-treated PC12 cells. Moreover, our in vivo findings demonstrated that administration of quercetin also relieved 6-OHDA-induced progressive PD-like motor behaviors, mitigated neuronal death and reduced mitochondrial damage and α-synuclein accumulation in PD rats. Furthermore, the neuroprotective effect of quercetin was suppressed by knockdown of either Pink1 or Parkin .

No abstract

No abstract

Low levels of serum vitamin D are common in patients with mood disorders and stroke. It has been shown that low levels of serum vitamin D indicate a risk of depression in post-stroke subjects. Our aim was to determine the relationship between vitamin D and post-stroke anxiety (PSA).A consecutive series of 226 first acute ischemic stroke patients were recruited and followed up for 1 month. Serum levels of vitamin D were measured within 24 hours of admission. Patients with significant clinical symptoms of anxiety and a Hamilton anxiety scale score >7 were diagnosed as having PSA. In addition, 100 healthy subjects were recruited as controls and underwent measurements of serum vitamin D.A total of 60 patients (26.55%) showed anxiety at 1 month. Both PSA patients and non-PSA patients had lower serum levels of vitamin D than healthy subjects. A significant relationship was found between PSA and serum levels of vitamin D. Low serum levels of vitamin D (≤38.48 nmol/L) were independently associated with the development of PSA (OR: 2.49, 95% CI: 1.21–5.13, P = 0.01).Serum vitamin D status is related to the occurrence of anxiety in post-stroke patients and may be an independent risk factor of PSA after 1 month.