Synthesis of L-aspartic acid-based bimetallic hybrid nanoflowers to immobilize snailase for the production of rare ginsenoside compound K.

The conversion of the common ginsenoside Rb1 to the rare ginsenoside compound K (CK) using snailase (Sna) is an efficient method for industrial production. In order to improve the stability and recoverability of Sna during the catalytic conversion of ginsenosides, the cage-like immobilised Sna material ZIF-ZnCo-Sna and the hybrid nanoflower-based immobilised Sna material Asp@ZIF-ZnCo-Sna modified with L-aspartic acid (Asp) were synthesised using a one-step method. The addition of Asp provides a richer ligand pattern and the morphology of the material changed from a cage to a hybrid nanoflower. The modified hybrid nanoflower Asp@ZIF-ZnCo-Sna has a larger specific surface area, resulting in an enzyme loading of 142.57 mg g-1. The more abundant mesopores allowed the enzyme to maintain a good conformation and the enzyme activity was 79.8% of that of the free Sna. In addition, the total conversion rate of Asp@ZIF-ZnCo-Sna to ginsenoside Rb1 was as high as 88.35%, whereas that of ZIF-ZnCo-Sna was 79.12%. Moreover, after 6 cycles, the catalytic conversion of ZIF-ZnCo-Sna and Asp@ZIF-ZnCo-Sna and the crystalline shape remained the same, indicating that both composites have good stability and catalytic properties. This new approach of improving the MOF morphology and enzymatic activity by a one-step addition of small biological molecules provides a simple, rapid, and effective strategy for biocatalysis. It also provides a certain reference value for the immobilized Sna to produce rare ginsenoside CK.

Artemisinin exerts a protective effect in the MPTP mouse model of Parkinson's disease by inhibiting microglial activation via the TLR4/Myd88/NF-KB pathway.

AIMS: We performed cell and animal experiments to explore the therapeutic effect of artemisinin on Parkinson's disease (PD) and the TLR4/Myd88 signaling pathway. METHODS: C57 mice were randomly divided into the blank, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced and artemisinin-treated groups. Clinical symptoms, the number of dopaminergic (DAergic) neurons in the substantia nigra, and microglial cell activation were compared among the three groups. Subsequently, BV-2 cell activation and TLR4/Myd88 pathway component expression were compared among the blank, MPP+ -treated, artemisinin-treated, and TLR4 activator-treated groups. RESULTS: Behavioral symptoms were improved, the number of DAergic neurons in the substantia nigra of the midbrain was increased, and microglial cell activation was decreased in artemisinin-treated MPTP-induced PD model mice compared with control-treated MPTP-induced PD model mice (p < 0.05). The cell experiments revealed that artemisinin treatment reduced MPP+ -induced BV-2 cell activation and inhibited the TLR4/Myd88 signaling pathway. Moreover, the effect of artemisinin on the BV-2 cell model was inhibited by the TLR4 activator LPS (p < 0.05). CONCLUSION: Artemisinin may reduce damage to DAergic neurons in a PD mouse model by decreasing microglial activation through the TLR4-mediated MyD88-dependent signaling pathway. However, this finding cannot explain the relationship between microglia and DAergic neurons.