Biochemical and physical investigations on detoxification of ginkgo kernel juice using probiotic fermentation with macroporous resin addition

The toxicity of ginkgo kernel is a global concern,restricting its consumption as a medicinal food.This study focuses on eliminating the toxic components,specifically ginkgolic acid,from ginkgo kernel juice.The approach used was probiotic fermentation with autochthonous lactic acid bacteria combined with macroporous resin.Compared to using lactic acid fermentation alone,adding macroporous resin during probiotic fermentation significantly enhanced the removal of toxic ginkgolic acid and 4'-O-methylpyridoxine from ginkgo kernel juice.After 48 h of fermentation with macroporous resin,the contents of ginkgolic acid and 4'-O-methylpyridoxine decreased by more than 69%and 61%,respectively.Interestingly,the adsorption of microbial growth inhibitors,such as ginkgolic acid,4'-O-methylpyridoxine,and phenolics,by the resin did not hinder the growth of lactic acid bacteria or their metabolic activities involving organic acids and monosaccharides.The study further confirmed that microbial adsorption was the primary reason for removing ginkgolic acid during probiotic fermentation.Also,the adsorption mechanism of ginkgolic acid during probiotic fermentation with macroporous resin was explored.From a mass transfer perspective,incorporating macroporous resin during the probiotic fermentation of ginkgo kernel juice reduced the mass transfer resistance for surface diffusion.Consequently,this lowered the contribution of surface diffusion to the overall diffusion process and facilitated the efficient removal of toxic ginkgolic acid.This work can help to understand the physical mechanism regarding detoxification of ginkgo kernel juice by probiotic fermentation,and offer potential strategies to enhance the safety of ginkgo kernel products.

Thymosin Alpha-1 Inhibits Complete Freund’s Adjuvant-Induced Pain and Production of Microglia-Mediated Pro-inflammatory Cytokines in Spinal Cord

Activation of inflammatory responses regulates the transmission of pain pathways through an integrated network in the peripheral and central nervous systems.The immunopotentiator thymosin alpha-1(Tal)has recently been reported to have anti-inflammatory and neuroprotective functions in rodents.However,how Tα1 affects inflammatory pain remains unclear.In the present study,intraperitoneal injection of Tal attenuated complete Freund's adjuvant(CFA)-induced pain hypersensitivity,and decreased the up-regulation of pro-inflammatory cytokines(TNF-α,IL-1β,and IL-6)in inflamed skin and the spinal cord.We found that CFA-induced peripheral inflammation evoked strong microglial activation,but the effect was reversed by Tα1.Notably,Tα1 reversed the CFA-induced up-regulation of vesicular glutamate transporter(VGLUT)and down-regulated the vesicular γ-aminobutyric acid transporter(VGAT)in the spinal cord.Taken together,these results suggest that Tα1 plays a therapeutic role in inflammatory pain and in the modulation of microgliainduced pro-inflammatory cytokine production in addition to mediation of VGLUT and VGAT expression in the spinal cord.