Astragalin is a natural flavonoid,which is known for its diverse pharmacological applications such as anti-tumor.The many studies have found that Astragalin has great anti-tumor potential by regulating PI3K/Akt signal pathway,MAPKs signal pathway,JAK/STAT signal pathway,NF-κ B signal pathway,Notch1 pathway,microRNA expression,tumor invasion and metastasis.This article reviews the literature reports on anti-tumor signal pathway of Astragalin in recent years,analyzes and summarizes the pos-sible mechanisms by which each pathway induces tumor cell apoptosis,in order to provide experimental and theoretical basis for the development and utilization of Astragalin in anti-tumor signal pathways.

Objective:To investigate influences of ginsenoside Rg1 regulating miR-144-3p on neuroinflammation and blood-brain barrier damage in rats with experimental cerebral hemorrhage,and its regulation on formyl peptide receptor 2(FPR2)/p38 path-way.Methods:Ninety SD rats were randomly divided into control group,cerebral hemorrhage group,ginsenoside Rg1 low-dose group(10 mg/kg),ginsenoside Rg1 high-dose group(40 mg/kg),ginsenoside Rg1 high-dose+ago-miR-144-3p group(40 mg/kg ginseno-side Rg1+ago-miR-144-3p),with 18 mice in each group.Except for control group,experimental intracerebral hemorrhage rat model was constructed by injecting collagenase Ⅱ into right caudate nucleus,and then each group was given intraperitoneal administration and intracerebral injection as required.Neurological damage in rats was scored;rat brain water content was determined by dry-wet spe-cific gravity method;levels of TNF-α,IL-6 and IL-1β in rat brain tissues homogenate were determined by ELISA;ultrastructure around cerebral edema was observed by electron microscope;permeability of blood-brain barrier in rats was determined by Evans blue(EB)method;expressions of miR-144-3p/FPR2/p38 pathway were determined by qRT-PCR and Western blot.Results:Compared with control group,blood-brain barrier damage was aggravated in cerebral hemorrhage group,neurological function damage score,brain water content,miR-144-3p,TNF-α,IL-6,IL-1β,p38 mRNA,p-p38/p38 expressions in brain homogenate were increased(P<0.05),FPR2 mRNA and protein expressions were decreased(P<0.05);compared with cerebral hemorrhage group,blood-brain barrier damage was reduced in ginsenoside Rg1 low-dose group and ginsenoside Rg1 high-dose group,neurological function damage score,brain water content,miR-144-3p,TNF-α,IL-6,IL-1β,p38 mRNA,p-p38/p38 expressions in brain homogenate were decreased(P<0.05),FPR2 mRNA and protein expressions were increased(P<0.05);ago-miR-144-3p was able to reverse protective effects of gin-senoside Rg1 on blood-brain barrier and neuroinflammation in rats(P<0.05).Conclusion:Ginsenoside Rg1 may inhibit blood-brain barrier damage and neuroinflammation in rats by regulating miR-144-3p/FPR2/p38 axis.

Objective:To investigate the effect of the adoptive transfer of CD4+CD25+Foxp3+regulatory T cells ( iTregs) induced by 5-aza-2′-deoxycytidine (5AzaD) on pregnant outcome of the abortion-prone mice.Methods:Sixty cases of female CBA/J × male DBA/2J abortion-prone matings were taken as study group,the CD4+T cells from spleen of twenty female CBA/J mice were separated by magnetic activated cell sorting (MACS),5AzaD was applied to the conversion of CD4+CD25-T cells to iTregs,the expression of Foxp3 in Tregs was characterized by flow cytometry analysis before and after epigenetic modification.The purified iTregs were injected into abortion-prone mice on day 1 or 4 of pregnancy,respectively,which were used as therapy groups,and then the embryo resorption rate was counted on day 14 of pregnancy.Results:After the treatment of 5AzaD,the percentage of iTregs in CD4+T cells was (41.50±8.03)%.The embryonic absorption rates of the two therapy groups were 10.47%(on day 1 of pregnancy) and 21.69%(on day 4 of pregnancy) ,respectively ( P<0.05 ) .Conclusion: Epigenetic modication of CD4+CD25-T cells may solve the problem of nTregs deficiency,particularly adoptive therapy of 5AzaD-induced iTregs at early stage of pregnancy can maintain normal pregnancy.