Autoimmune diseases are one of the main diseases that endanger human health. Existing immunosuppressants such as cyclosporin often produce many adverse reactions and cause additional damage to the human body. Looking for new immunosuppressants with high efficiency and low toxicity has become a research hotspot.AstilbinAstilbin is a flavonoid glycoside extracted from traditional Chinese medicine such as Smilax cocos. Studies have shown that astilbin has significant immunosuppressive activity, including inhibition of contact dermatitis and liver injury caused by delayed hypersensitivity, and inhibition of collagen and adjuvant arthritis. However, it has no common toxic and side effects of existing immunosuppressants. Its immunosuppressive effect is selective, that is, it selectively inhibits activated T lymphocytes without affecting normal T lymphocytes and other tissue cells. This feature has not been reported in the past. Therefore, it is very important to study its selectivity. It is found that astilbin inhibits activated T cells by selectively inducing activated tapoptosis. Its mechanism is to activate the mitochondrial apoptosis pathway, cause baxq and bad in activated Jurkat cells to transfer to mitochondria, open the permeability pore (PTP) on the mitochondrial membrane, and release cytochrome c to induce apoptosis.

    Using affinity chromatography, proteins that can bind to astilbin were isolated from Jurkat cells activated by PHA (phytohemagglutinin). One of them was identified as heterogeneous  nuclear  ribonucleprotein  A1, hnrnp  A1, a member of hnRNP family.

    Recombinant expression of human hnrnp  The in vitro study of A1 egg autoantibody and anti astilbin polyclonal antibody, and the 3D structure simulation by molecular docking software confirmed that astilbin could interact with hnrnp  A1 is combined with each other. Meanwhile, astilbin affects hnrnp  The results of A1 fluorescence quenching showed that the interaction between them may be related to the multiple hydroxyl groups carried by astilbin.