Zhu Y.,Nanjing Research Institute for Comprehensive Utilization of Wild Plants |
Zhao B.,Nanjing Research Institute for Comprehensive Utilization of Wild Plants |
Huang X.,Nanjing Research Institute for Comprehensive Utilization of Wild Plants |
Chen B.,Nanjing Research Institute for Comprehensive Utilization of Wild Plants |
Qian H.,Nanjing Research Institute for Comprehensive Utilization of Wild Plants
Journal of Microbiology and Biotechnology | Year: 2014
The natural crosslinking agent genipin has been applied widely in biomedicines and foods nowadays. Because of the special hemiacetal ring structure in its molecule, it can only be prepared by hydrolysis of geniposide according to biocatalysis. In this research, strategies including aqueous-organic biphasic catalysis and substrate fed-batch mode were adopted to improve the biocatalysis process of genipin. A 10 L ethyl acetate-aqueous biphasic system with geniposide fed-batch led to a satisfying genipin yield. With Fusarium solani ACCC 36223, 15.7 g/l genipin in the ethyl acetate phase was obtained, corresponding to space-time yields of 0.654 g l-1 h-1. © 2015 by The Korean Society for Microbiology and Biotechnology.
PubMed | Nanjing Research Institute for Comprehensive Utilization of Wild Plants and Nanjing University
Type: | Journal: Scientific reports | Year: 2016
Sulforaphane, a naturally occurring compound found in cruciferous vegetables, has been shown to be neuroprotective in several neurological disorders. In this study, we sought to investigate the potential protective effects and associated molecular mechanisms of sulforaphane in an in vivo Parkinsons disease (PD) model, based on rotenone-mediated neurotoxicity. Our results showed that sulforaphane inhibited rotenone-induced locomotor activity deficiency and dopaminergic neuronal loss. Additionally, sulforaphane treatment inhibited the rotenone-induced reactive oxygen species production, malondialdehyde (MDA) accumulation, and resulted in an increased level of total glutathione and reduced glutathione (GSH): oxidized glutathione (GSSG) in the brain. Western blot analysis illustrated that sulforaphane increased the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinone oxidoreductase (NQO1), the latter two of which are anti-oxidative enzymes. Moreover, sulforaphane treatment significantly attenuated rotenone-inhibited mTOR-mediated p70S6K and 4E-BP1 signalling pathway, as well as neuronal apoptosis. In addition, sulforaphane rescued rotenone-inhibited autophagy, as detected by LC3-II. Collectively, these findings demonstrated that sulforaphane exert neuroprotective effect involving Nrf2-dependent reductions in oxidative stress, mTOR-dependent inhibition of neuronal apoptosis, and the restoration of normal autophagy. Sulforaphane appears to be a promising compound with neuroprotective properties that may play an important role in preventing PD.
PubMed | Nanjing Research Institute for Comprehensive Utilization of Wild Plants
Type: Journal Article | Journal: Acta crystallographica. Section E, Structure reports online | Year: 2011
In the crystal structure of the title compound, C(8)H(12)O(6), mol-ecules are linked to each other by O-HO hydrogen bonding.