Electrochemical CO2 reduction (CO2R) powered by renewable energy to convert CO2 molecules into formate is of great interest. It is still challenging to develop an efficient CO2R catalyst with high selectivity. Herein, we adjust the adsorption states of CO2 – intermediates to improve the selectivity of CO2 toward formate by doping S to Cu-based electrocatalysts. It can be found that S doping could stabilize the reductive-state Cu as the active site for CO2R. The vibration models of CO2 – intermediates within in situ Raman spectroscopy reveal that the selectivity improvement is ascribed to the change of the adsorption state from coexisting O*CO– and OC*O*– to the dominating OC*O*–. The electrocatalyst manifests high selectivity and activity toward formate (maximum Faradaic efficiency as high as 76.5% and maximum partial current density 21.06 mA cm–2).

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Alcoholic liver injury, known as the most general result of chronic alcohol intake, is induced by inflammatory responses, which is activated by intestine-derived endotoxins formed from intestinal dysbiosis. The hepatoprotective activity of rice bran phenolic extract (RBPE) on ethanol-fed mice was investigated for the first time in this study, and the underlying mechanism was explored from gut microbiota, barrier function, and hepatic inflammation. Mice were fed an alcohol-containing liquid diet alone or in mixture with RBPE for 8 weeks. RBPE treatment mitigated ethanol-induced liver damage, evidenced by the declined lipid profile levels and hepatic function markers. Moreover, ethanol intake induced intestinal microbiota dysbiosis, which was attenuated by RBPE supplementation. RBPE treatment improved the alcohol-induced decrease in the expression of ZO-1, Claudin-1, Claudin-4, and Reg3g, revealing the ameliorative effect of RBPE on intestinal barrier dysfunction. Furthermore, RBPE treatment repressed the alcohol-induced trigger of the hepatic endotoxin–TLR4–NF-κB pathway, followed by the mitigated liver inflammation. The findings indicate that RBPE supplementation ameliorates intestinal microbiota dysbiosis and barrier dysfunction, inactivates the endotoxin–TLR4–NF-κB pathway, and represses inflammatory responses in liver, and therefore, intake of RBPE or brown rice may be an effective way to mitigate alcoholic liver injury.

Mitochondria play an important role in the initiation and development of alcoholic liver disease (ALD). Our previous studies found lychee pulp phenolic extract (LPPE) exerted protective effect against ALD partly by inhibiting fatty acid β-oxidation, and phenolic-rich lychee pulp extract improved restraint stress-induced liver injury by inhibiting mitochondrial dysfunction. The aim of this study was to investigate whether LPPE exerted protective effect against ALD via modulating mitochondrial function. The mice were treated with an ethanol-containing liquid diet alone or in combination with LPPE for 8 weeks. LPPE supplementation significantly alleviated hepatic steatosis, suppressed serum aspartate aminotransferase activity, and decreased triglyceride levels in serum and liver. On the basis of lipid peroxidation and antioxidant enzyme analyses, LPPE supplementation inhibited serum and hepatic oxidative stress. Moreover, LPPE supplementation significantly suppressed mitochondrial 8-hydroxy-2'-deoxyguanosine level, and increased mitochondrial membrane potential, mitochondrial DNA content, activities of mitochondrial complexes I and IV, and hepatic ATP level. Furthermore, LPPE supplementation significantly inhibited cytoplasmic cytochrome c level and caspase-3 activity, repressed Bax expression and Bax/Bcl-2 ratio, and increased Bcl-2 expression in liver. In summary, LPPE exerts beneficial effects against alcoholic liver injury by alleviating mitochondrial dysfunction.

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The tumor suppressor p53 is at the hub of cellular signaling networks that are activated by stress signals including DNA damage. In the present study, we showed that programmed cell death 5 (PDCD5) bound to p53 by glutathione S-transferase (GST)-pulldown, co-immunoprecipitation and co-localization assays. PDCD5 enhanced the stability of p53 by antagonizing Mdm2-induced p53 ubiquitination, nuclear export and proteasomal degradation. We also found that PDCD5 could dissociate the interaction between p53 and Mdm2 and interact with Mdm2 directly to promote its degradation. In cells with or without induction of DNA damage, knockdown of PDCD5 by RNA interference decreased the p53 phosphorylation at Ser9, 20 and 392 residues, as well as the expression of p21 protein. Additionally, chromatin immunoprecipitation assays showed an up-regulated association of PDCD5 at the p53BS2 site of the p21 promoter during DNA damage. Cell cycle analysis also indicated that PDCD5 was required in G1 phase cell arrest during DNA damage. In summary, PDCD5 may contribute to maintain a basal pool of p53 proteins in unstressed conditions, but upon DNA damage it functions as a co-activator of p53 to regulate transcription and cell cycle arrest.

Liver injury is the most common consequence of alcohol abuse, which is promoted by the inflammatory response triggered by gut-derived endotoxins produced as a consequence of intestinal microbiota dysbiosis and barrier dysfunction. The aim of this study was to investigate whether modulation of intestinal microbiota and barrier function, and liver inflammation contributes to the hepatoprotective effect of lychee pulp phenolic extract (LPPE) in alcohol-fed mice. Mice were treated with an ethanol-containing liquid diet alone or in combination with LPPE for 8 weeks. LPPE supplementation alleviated ethanol-induced liver injury and downregulated key markers of inflammation. Moreover, LPPE supplementation reversed the ethanol-induced alteration of intestinal microbiota composition and increased the expression of intestinal tight junction proteins, mucus protecting proteins, and antimicrobial proteins. Furthermore, in addition to decreasing serum endotoxin level, LPPE supplementation suppressed CD14 and toll-like receptor 4 expression, and repressed the activation of nuclear factor-κB p65 in the liver. These data suggest that intestinal microbiota dysbiosis, intestinal barrier dysfunction, and liver inflammation are improved by LPPE, and therefore, the intake of LPPE or Litchi pulp may be an effective strategy to alleviate the susceptibility to alcohol-induced hepatic diseases.