RESUMEN
Synthetic biohybrid systems by coupling artificial system with nature's machinery may offer a disruptive solution to address the global energy crisis. We developed a versatile electroenzymatic pathway for the continuous synthesis of valuable chemicals, facilitated by formate-driven NADH regeneration. Utilising a bismuth electrocatalyst, we achieved stable CO2 reduction to formate with approximately 90% Faraday efficiency at a current density of 150 mA cm-2. The generated formate acts as a mediator to regenerate NADH, which is then coupled with immobilised redox enzymes-alcohol dehydrogenase (ADH), L-lactate dehydrogenase (LDH), and L-glutamate dehydrogenase (GDH)-to produce targeted chemicals at significant rates and exceptionally high turnover numbers (1.8×106 to 3.1×106). These achievements not only underscore the efficiency of the system but also its practical applicability in industrial settings. By leveraging in situ generated formate, this innovative approach demonstrates the potential of integrating electrocatalysis with enzymatic reactions for sustainable and efficient chemical production on a practical scale.
RESUMEN
The conversion of CO2 into value-added chemicals and fuels using stable, cost-effective, and eco-friendly metal-free catalysts is a promising technology to mitigate the global environmental crisis. In the Calvin cycle of natural photosynthesis, CO2 reduction (CO2R) is achieved using the cofactor NADPH as the reducing agent through 2e-/1H+ or H- transfer. Consequently, inspired by NAD(P)H, a series of organohydrides with adjustable reducibility show remarkable potential for efficient metal-free CO2R. In this review, we first summarize the photosensitizers for NAD(P)H regeneration and list the representative photoenzyme CO2R system. Then, we introduce the NAD(P)H-inspired organohydrides and their applications in redox reactions. Furthermore, we discuss recent progress and breakthroughs by utilizing organohydrides as metal-free CO2R catalysts. Moreover, we delve into the reaction mechanisms and applications of these organohydrides, shedding light on their potential as sustainable alternatives to metal-based CO2R catalysts. Finally, we offer insights into the prospects and potential directions for advancing this intriguing avenue of organohydride-based catalysts for CO2R.
RESUMEN
Macrophages are involved in hepatocyte steatosis and necroinflammation and play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Impaired autophagy function (decreased autophagy or blocked autophagic flow) leads to cell damage and death and promotes NAFLD progression. The experimental and clinical research of glycyrrhetinic acid (GA) in the treatment of NAFLD has gradually attracted attention with clear pharmacological activities such as immune regulation, antiviral, antitumor, antioxidant, liver protection, and anti-inflammatory. However, the effects of GA on the STAT3-HIF-1α pathway and autophagy in macrophages are still unclear, and its mechanism of action in the treatment of NAFLD remains to be further elucidated. We constructed a NAFLD mouse model through a high-fat and high-sugar diet to investigate the therapeutic effects of GA. The results showed that GA reduced weight, improved the pathological changes and hepatic lipid deposition of liver, and abnormally elevated the levels of serum biochemical (AST, ALT, TG, T-CHO, LDL-C, and HDL-C) and inflammatory indexes (IL-1ß, IL-4, IL-6, MCP-1, and TNF-α) in NAFLD mice. Further examination revealed that GA ameliorates excessive hepatic macrophage infiltration and hepatocyte apoptosis. The results of the cell experiments further elaborated that GA modulated the PA-induced macrophage STAT3-HIF-1α pathway and ameliorated impaired autophagic flux (blockade of autophagosome-lysosome fusion) and overactivation of inflammation. Excessive hepatocyte apoptosis caused by the uncontrolled release of inflammatory cytokines was also suppressed by GA. Conclusion: This study demonstrated that GA could regulate the STAT3-HIF-1α pathway of macrophages, ameliorate the impaired autophagy flux, and reduce the excessive production of inflammatory cytokines to improve the excessive apoptosis of liver cells, thus playing a therapeutic role on NAFLD.