Serum and glucocorticoid-inducible kinases (SGKs) are serine threonine protein kinases involved in the regulation of multiple signal transduction pathways in vivo. SGKs include SGK1, SGK2 and SGK3. SGK1 plays a crucial role in the development of diseases such as digestive inflammation and tumors by regulating inflammatory and immune responses through phosphorylation. This article briefly introduces the structure and function of SGK1, and describes the research progress and clinical significance of SGK1 in digestive diseases.

The development of inflammatory bowel diseases (IBD) is associated with genetics, environment, immune abnormalities, and intestinal flora, including ulcerative colitis (UC) and Crohn′s disease (CD). Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that promotes the expression of multiple genes in response to the hypoxic environment, and its roles in regulating intestinal barrier function, intestinal metabolism, and inflammatory and immune responses are research hotspots. This article reviews the role of HIF-1α in IBD by analyzing the relationships between HIF-1α and intestinal epithelial barrier and inflammatory response to provide new ideas for the clinical treatment of IBD.

The development of inflammatory bowel diseases (IBD) is associated with genetics, environment, immune abnormalities, and intestinal flora, including ulcerative colitis (UC) and Crohn′s disease (CD). Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that promotes the expression of multiple genes in response to the hypoxic environment, and its roles in regulating intestinal barrier function, intestinal metabolism, and inflammatory and immune responses are research hotspots. This article reviews the role of HIF-1α in IBD by analyzing the relationships between HIF-1α and intestinal epithelial barrier and inflammatory response to provide new ideas for the clinical treatment of IBD.

Objective To investigate the effect of p15~(INK4B)(p15)gene transfection on the proliferation of pancreatic cancer cell line BxPC3.Methods In p15 transfection group.pCDNA3.1(+)p15 was transfected into BxPC3 cell by the vector of Lipofectamine2000.In empty plasmid transfection group, pCDNA3.1(+)neo was transfected into BxPC3 cell with the sa/ne method as a blank control group.In non-transfection group.the BxPC3 cell was not transfected as a negative control group.The p15 mRNA expressions were assayed by RT-PCR,and p15 protein expressions were assayed by Western blot.The proliferation was determined by MTY assay,ultra-structure changes were measured by transmission electron microscope.Cell cycle and apoptosis were measured by flow cytometry.Results In the pCDNA3.1(+)p15 transfeetion group,the expression of p15 mRNA and protein were resumed.Since the 2nd day of culture,the growth of pCDNA3.1(+)p15 transfeetion group was inhibited,till the 7th day,the inhibitory rate was 47.9%,G_0/G_1 Dhase cell accounted for(61.56±3.96)% of all the cells,which was significantly higher than(47.44±6.35)%ofthe black control groups and(49.22±7.23)%0f tlle negative control group(P<0.05).G_1apoptosis peak occurred and the apoptosis rate was(5.27±1.04)%in pCDNA3.1(+)p15 transfection group,which was significantly higher than(0.11±0.06)% of the black control groups and(0.09±0.07)% of the negative control group(P<0.05).Apoptosis was also observed by transmission electron microscope in the pCDNA3.1(+)-p15 transfection group cells.Conclusions After p15 gene transfection,BLPC3 cell proliferation could be significantly inhibited and apoptosis could be induced.