Biological valorization of lignin to flavonoids.

Lignin is the most affluent natural aromatic biopolymer on the earth, which is the promising renewable source for valuable products to promote the sustainability of biorefinery. Flavonoids are a class of plant polyphenolic secondary metabolites containing the benzene ring structure with various biological activities, which are largely applied in health food, pharmaceutical, and medical fields. Due to the aromatic similarity, microbial conversion of lignin derived aromatics to flavonoids could facilitate flavonoid biosynthesis and promote the lignin valorization. This review thereby prospects a novel valorization route of lignin to high-value natural products and demonstrates the potential advantages of microbial bioconversion of lignin to flavonoids. The biodegradation of lignin polymers is summarized to identify aromatic monomers as momentous precursors for flavonoid synthesis. The biosynthesis pathways of flavonoids in both plants and strains are introduced and compared. After that, the key branch points and important intermediates are clearly discussed in the biosynthesis pathways of flavonoids. Moreover, the most significant enzyme reactions including Claisen condensation, cyclization and hydroxylation are demonstrated in the biosynthesis pathways of flavonoids. Finally, current challenges and potential future strategies are also discussed for transforming lignin into various flavonoids. The holistic microbial conversion routes of lignin to flavonoids could make a sustainable production of flavonoids and improve the feasibility of lignin valorization.

[Study on protective effect of monosialoganglioside (GM1) on injury induced by oxygen glucose deprivation/reperfusion in rat hippocampal slices].

AIM: To investigate the protective effect of monosialoganglioside (GM1) on injury induced by oxygen glucose deprivation/reperfusion (OGD/Rep) in rat hippocampal slices. METHODS: The protective effects of GM1 on hippocampal slices after OGD/Rep were observed by detecting the light transmittance (LT) changes of rat hippocampal slices and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining of rat hippocampal slices. RESULTS: (1) In four groups treated with 0 (control), 0.1, 1.0, 10 micromol/L GM1, the peak of light transmittance (LT) in the slices treated with 1.0 micromol/L GM1 was significantly lower than that of the control and the group treated with 0.10 micromol/L GM1 (P < 0.01, ANOVA), while the peak of LT in the slices treated with 10.0 micromol/L GM1 was significantly lower than that of the other groups (P < 0.01, ANOVA). The time to reach the peak of LT in four groups was significantly different from each other (P < 0.05, Kruskal-Wallis test). The time to reach the peak of LT in the group treated with 1 micromol/L GM1 was the significantly longer than that in the control (P < 0.01, Mann-Whitney U test). (2) There was characteristic dose-response relationship between GM1 and TTC staining of rat hippocampal slices. In the five groups, treated with 0 (control), 0.01, 0.1, 1.0, 10 micromol/L GM1 respectively, TTC staining in the group treated with 1 micromol/L GM1 was the deepest (P < 0.05 vs. control, 0.01 and 0.1 micromol/L GM1 group, ANOVA), and the next was in the group treated with 10 micromol/L GM1 (P < 0.05 vs. control and 0.01 micromol/L GM1 group, ANOVA). CONCLUSION: GM1 could protect injury induced by OGD/Rep in rat hippocampal slices effectively in vitro.