Fibroblast growth factors (FGFs) and their receptors, fibroblast growth factor receptors (FGFRs), constitute an essential signaling system that is widely involved in development, tissue homeostasis, and metabolic regulation. In recent years, advances in cryo-electron microscopy and protein engineering have shifted FGF-FGFR research from the traditional receptor activation paradigm toward a new framework centered on protein-protein interactions and receptor conformation-mediated signaling bias. This review summarizes the structural basis of FGF-FGFR protein interactions, with particular emphasis on the asymmetric dimer model, the distinct receptor recognition mechanisms of paracrine and endocrine FGFs, and recent progress in the receptor dimerization threshold model. It further discusses the molecular mechanisms underlying FGFR signaling bias and summarizes recent progress in the design of engineered FGF analogs and FGFR agonists, aiming to provide new theoretical insights for precision therapies for metabolic diseases.

Objective: To study the toxicological effects of Nao-de-kang on rats. Methods: According to the digital table, SD rats were randomly divided into blank group and Nao-de-kang small dose group(3.85g/kg), high dose group(7.71g/kg) and maximum tolerated dose group(77.14g/kg), 20 rats in each group, half male and half female.All groups were treated for 12 weeks, and the maximum tolerated dose group was treated for 1 week.The animal activity during treatment, the blood routine indicators, blood biochemical index and the organs for pathological examination were recorded and compared. Results: There was no mortality in the dose group of rats in the experimental period.The weights of 4 groups had no statistically significant differences during treatment(F=0.688, 0.540, 0.121, 0.065, 0.128, 0.239, 0.199, 0.378, 0.127, 0.446, 0.906 and 0.665, P=0.562, 0.585, 0.886, 0.937, 0.880, 0.788, 0.820, 0.687, 0.881, 0.642, 0.410 and 0.518), male and femal′s red blood cell(RBC)(♀: F=0.178, P=0.910, ♂: F=0.119, P=0.948), hemoglobin(HGB)(♀: F=0.046, P=0.987, ♂: F=0.072, P=0.975), hematokrit(HCT)(♀: F=0.126, P=0.944, ♂: F=0.054, P=0.983), platelet(PLT)(♀: F=0.515, P=0.675, ♂: F=0.500, P=0.685), white blood cell(WBC)(♀: F=0.078, P=0.972, ♂: F=0.057, P=0.982), eosnophils(Eos)(♀: F=0.078, P=0.972, ♂: F=0.057, P=0.982), lymphocyte(Lym)(♀: F=0.078, P=0.972, ♂: F=0.057, P=0.982), neutrophilic granulocyte(Neu)(♀: F=0.134, P=0.939, ♂: F=0.090, P=0.999), alanine aminotransfease (ALT)(♀: F=0.572, P=0.637, ♂: F=0.200, P=0.896), aspartate aminotransferase(AST)(♀: F=0.572, P=0.637, ♂: F=0.200, P=0.896), total protein(TP)(♀: F=0.665, P=0.579, ♂: F=0.343, P=0.795), albumin(ALB)(♀: F=0.533, P=0.663, ♂: F=0.668, P=0.577), triglyceride(TG)(♀: F=0.843, P=0.480, ♂: F=0.561, P=0.644), cholesterol(CHOL)(♀: F=0.245, P=0.864, ♂: F=0.046, P=0.987), glucose(GLU)(♀: F=0.216, P=0.884, ♂: F=0.095, P=0.963), urea nitrogen(BUN)(♀: F=0.172, P=0.914, ♂: F=0.203, P=0.894)and creatinine(Cr)(♀: F=0.172, P=0.914, ♂: F=0.203, P=0.894) had no statistically significant differences. Conclusion Nao-de-kang has no obvious side effect.

Objective To observe the effect of Xinjia-Liangfu(XJLF)formula on human gastric cancer(SGC-7901)tumor growth in nude mice and its impact on survivinand Caspase-3 expression in tumor tissue. Methods The animal model of SGC-7901 xenografted nude mice was established, and all the mice were randomly divided into 6 groups, namely model control group, 5-Fu group, XJLF formula high-dose group, XJLF formula medium-dose group , XJLF formula low-dose group and drug combination group(XJLFformula medium-dose and 5-Fu). After 10 days of continuous treatment, tumor inhibition rate was calculated and the expression of Survivin and Caspase-3 was detected by immunohistochemistry techniques. Results The tumor inhibition rates of 5-Fu group, XJLF formula high-dose group, XJLF formula medium-dose group, XJLF formula low-dose group and drug combination group were 55.03%, 56.38%, 41.23%, 23.09%and 60.28%respectively, and the tumor inhibition rate of drug combination group was significantly increased compared to the model control group(P<0.05), 5-Fu group(P<0.05)and XJLF high-dose group(P<0.05) Meanwhile, the Caspase-3 expression was significantly up-regulated and the Survivin expression was significantly down-regulated in drug combination group(Caspase-3 was 77 539.74±50 912.5, Suvivin was 35 709.1±10404.4)compared to the model control group(Caspase-3 was 18 464.71±7 537.01,Suvivin was 63 449.4±50 498.8), P<0.05 or 0.01, 5-Fu groupCaspase-3 was (47 198.89±10 751.2), Suvivin was(37 016.8±6 024.4), P<0.05 or 0.01and XJLF formula high-dose groupCaspase-3was (44213.57±7041.6), Suvivin was (38811.1±7313.0)respectively. Conclusion The tumor inhibition rate of drug combination group was higher than XJLF formula high-dose group and 5-Fu group. Also combination group hadstronger effect compared to model control group in terms of down-regulation of Caspase-3 expression and up-regulation of Survivin expression, which indicates a benefit ofXJLF and 5-Fu combination treatment.