Objective To investigate the macrophages (Mφ) phenotype mechanism in acute kidney injury caused by severe acute pancreatitis (SAP).Methods Sixty-four male Wistar rats were randomly divided into control group (SO) and SAP group (n =32 in each group).SAP rat model was made by retrograde cholangiopancreatic injection of 5％ sodium taurocholate.At 2,6,12 and 24 h after modeling,the samples of blood and kidney tissue were collected.The levels of blood urea nitrogen (BUN) and creatinine (Cr) were detected by using automatic biochemical analyzer.The expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA of kidney tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR).The levels of CD68,iNOS and Arg-1 were measured by Western blot.Results In the SAP group at each interval,BUN and Cr concentrations were significantly higher than those of the control group (P ＜ 0.01,P ＜ 0.05) ; Compared with the control group,the expressions of IL-12,TNF-α,IL-10 and TGF-β mRNA in renal tissue of SAP group were significantly higher (P ＜ 0.01,P ＜ 0.05).In the SAP group,the levels of CD68,iNOS and Arg-1 were higher than those in the control group.Conclusions Inflammation and inflammatory imbalances may be pathological factors of acute kidney injury following SAP.

Objective To investigate the effect of triggering receptor expression in myeloid cells-1 (TREM-1) on intestinal macrophage apoptosis in rat.Methods In vitro,the achieved rat intestinal macrophages were divided into 3 groups:control group,LPS (Lipopolysaccharides) group and LPS + LP17 group (n =6 holes of culture plate in each).The concentrations of LPS and LP17 were 1 mg/L and 0.1 mg/L,respectively.The intestinal macrophage apoptosis was measured by using TUNEL kit and flow cytometry after culture for 6 h.All data were statistically analyzed using SPSS 18.0 software.Results The shape and growth of rat intestinal macrophages were quite favorable after culture.The membrane marker of intestinal macrophages,CD14 was clearly observed under immunofluorescence.After macrophage was treated with specific procedure,the cell apoptosis found in LPS group (44.33 ± 7.74)％ was significantly higher than that in control group (19.17 ± 6.01) ％ (P=0.000) measured by TUNEL;the cell apoptosis in LPS +LP17 group (28.33 ± 6.53)％ apparently reduced compared with LPS group (44.33 ±7.74) ％ (P =0.004);there was no significant difference in cell apoptosis between control group (19.17 ± 6.01) ％ and LPS + LP17 group (28.33 ± 6.53) ％ (P =0.050).By flow cytometry,the apoptotic cells in LPS group (16.47 ± 1.66) ％ was significantly increased compared with control group (7.70 ± 1.52) ％ (P =0.000);apoptotic cells in LPS + LP17 group (11.47 ± 3.12) ％ was significantly reduced in comparison with LPS group (16.47 ± 1.66) ％ (P =0.018).There was no significant difference in apoptotic cells between control group (7.70±1.52)％ and LPS + LP17 group (11.47±3.12) ％ (P =0.061).Conclusion LP17 can inhibit TREM-1 expression in intestinal macrophages and reduce intestinal macrophage apoptosis.

Objective To investigate the effect of solasonine,an active component of Solanum nigrum,on proliferation and apoptosis of non-small cell lung cancer PC9 cells.Methods PC9 cells were treated with 2,5,10,15,20,or 25 μmol/L solasonine,and the changes in cell proliferation were examined using CCK-8 assay.Tetramethyl rhodamine ethyl ester(TMRE)was used to detect the changes in mitochondrial membrane potential,and caspase-3/7 detection kit and GreenNuc? caspase-3/Annexin V-mCherry kit for live cell were used to analyze the changes in caspase-3 of the cells.Annexin V-FITC/PI double staining was employed to analyze the apoptosis rate of the cells.The effect of PTEN inhibitors on solasonine-induced cell apoptosis was examined by detecting apoptosis-related protein expressions using Western blotting.Results Solasonine treatment for 24,48,and 72 h significantly lowered the viability of PC9 cells.The cells treated with solasonine for 24 h showed significantly decreased mitochondrial membrane potential and increased cell apoptosis with enhanced caspase-3/7 and caspase-3 activities and expression of cleaved caspase-3.Solasonine treatment significantly decreased phosphorylation levels of PI3K and Akt,increased the protein expressions of PTEN and Bax,and lowered the expression of Bcl-2 protein in the cells.Conclusion Solasonine inhibits proliferation and induces apoptosis of PC9 cells by regulating the Bcl-2/Bax/caspase-3 pathway and its upstream proteins.

Objective To investigate the effect of solasonine,an active component of Solanum nigrum,on proliferation and apoptosis of non-small cell lung cancer PC9 cells.Methods PC9 cells were treated with 2,5,10,15,20,or 25 μmol/L solasonine,and the changes in cell proliferation were examined using CCK-8 assay.Tetramethyl rhodamine ethyl ester(TMRE)was used to detect the changes in mitochondrial membrane potential,and caspase-3/7 detection kit and GreenNuc? caspase-3/Annexin V-mCherry kit for live cell were used to analyze the changes in caspase-3 of the cells.Annexin V-FITC/PI double staining was employed to analyze the apoptosis rate of the cells.The effect of PTEN inhibitors on solasonine-induced cell apoptosis was examined by detecting apoptosis-related protein expressions using Western blotting.Results Solasonine treatment for 24,48,and 72 h significantly lowered the viability of PC9 cells.The cells treated with solasonine for 24 h showed significantly decreased mitochondrial membrane potential and increased cell apoptosis with enhanced caspase-3/7 and caspase-3 activities and expression of cleaved caspase-3.Solasonine treatment significantly decreased phosphorylation levels of PI3K and Akt,increased the protein expressions of PTEN and Bax,and lowered the expression of Bcl-2 protein in the cells.Conclusion Solasonine inhibits proliferation and induces apoptosis of PC9 cells by regulating the Bcl-2/Bax/caspase-3 pathway and its upstream proteins.

Brown adipose tissue (BAT) holds great promise for the prevention and treatment of metabolism diseases through thermoregulation. Polycystic ovary syndrome (PCOS) is a complex condition with anovulation, hyperandrogenism, and polycystic ovaries, and also manifests glucolipid metabolic disorders. Recent researches have shown that transplantation of BAT into a PCOS rat could significantly alleviate the phenotypes. This article reviews the role of BAT in pathogenesis of PCOS, which may provide information for prevention and treatment of PCOS.