Piceatannol Protects PC-12 Cells against Oxidative Damage and Mitochondrial Dysfunction by Inhibiting Autophagy via SIRT3 Pathway.

Oxidative stress has been identified as a major cause of cellular injury in a variety of neurodegenerative disorders. This study aimed to investigate the cytoprotective effects of piceatannol on hydrogen peroxide (H2O2)-induced pheochromocytoma-12 (PC-12) cell damage and explore the underlying mechanisms. Our findings indicated that piceatannol pre-treatment significantly attenuated H2O2-induced PC-12 cell death. Furthermore, piceatannol effectively improved mitochondrial content and mitochondrial function, including enhancing mitochondrial reactive oxygen species (ROS) elimination capacity and increasing mitochondrial transcription factor (TFAM), peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α) and mitochondria Complex IV expression. Meanwhile, piceatannol treatment inhibited mitochondria-mediated autophagy as demonstrated by restoring mitochondrial membrane potential, reducing autophagosome formation and light chain 3B II/I (LC3B II/I) and autophagy-related protein 5 (ATG5) expression level. The protein expression level of SIRT3 was significantly increased by piceatannol in a concentration-dependent manner. However, the cytoprotective effect of piceatannol was dramatically abolished by sirtuin 3 (SIRT3) inhibitor, 3-(1H-1,2,3-Triazol-4-yl) pyridine (3-TYP), which led to an exacerbated mitochondrial dysfunction and autophagy in PC-12 cells under oxidative stress. In addition, the autophagy activator (rapamycin) abrogated the protective effects of piceatannol on PC-12 cell death. These findings demonstrated that piceatannol could alleviate PC-12 cell oxidative damage and mitochondrial dysfunction by inhibiting autophagy via the SIRT3 pathway.

Quinoa bran soluble dietary fiber ameliorates dextran sodium sulfate induced ulcerative colitis in BALB/c mice by maintaining intestinal barrier function and modulating gut microbiota.

To clarify the effect of quinoa bran soluble dietary fiber (QBSDF) on gut inflammation and homeostasis, ulcerative colitis (UC) mice induced by dextran sodium sulfate (DSS) were fed QBSDF for four weeks. Histological staining, immunofluorescence, western blot and 16S rRNA sequencing analysis were carried out to investigate the action mechanism of QBSDF. Results showed that QBSDF alleviated DSS-induced colitis symptoms accompanied by significant mitigation of colon shortening and colonic epithelial damage. Moreover, QBSDF supplementation downregulated the mRNA and protein expression level of TNF-α and IL-1ß, while elevated the expression of tight junction proteins, and significantly reduced colonic cells apoptosis. In addition, the diversity and abundance of gut microbiota in QBSDF fed mice were significantly increased compared to that of UC mice. Moreover, QBSDF notably increased the abundance of Firmicutes at phylum level, while decreased the abundance of Bacteroidetes and pathogenic Helicobacter. Besides, the levels of short-chain fatty acids, especially acetic acid and butyric acid were significantly increased by QBSDF administration. These findings suggested the promising potential of QBSDF as a functional food ingredient to prevent ulcerative colitis through maintaining intestinal barrier function and modulating gut microbiota.