1.Protective role of ERp46 in palmitic acid-induced endoplasmic reticulum stress
Danling CHEN ; Jingnan XIANG ; Liyong YANG
Chinese Journal of Endocrinology and Metabolism 2012;(12):1012-1015
Detection of the possible role of ERp46,new endoplasmic reticulum protein,on palmitic acid-inducedendoplasmic reticulum stress-apoptosis pathway in βTC6 cells for the new treatment of type 2 diabetes.Results showed that ERp46 played a protective role in palnutic acid-induced cell apoptosis by decreasing the endoplasmic reticulum stress response through three pathway.
2.The relationship between HBV genotypes and anti-virus therapeutic efficacy of interferon
Yunzhen SHI ; Zhaoxia LI ; Jingnan LI ; Tiangao CAO ; Xiang CHEN ; Yajun SONG ; Suping DU ; Yaner WANG
Chinese Journal of Primary Medicine and Pharmacy 2009;16(8):1388-1389
Objective To study the effects of Interferon(IFN)in chronic hepatitis B patients genotype B and C.Methods 20 cases were genotype B ,23 cases were genotype C,all the patients were treated with 5 million units of IFN-a-lb,im,qod,for 12 months,viral markers,liver function and adverse drug reactions were observed.Results There was no statistically significant difference between B,C genotype in the negative conversion rate of HBV-DNA (60.0% ,39.1%),the negative conversion rate of HBeAg(42.9% ,30.8%),anti-HBe seroconversion rate(35.7% ,23.1 %)and the rate ALT normalization(85.0% ,73.9%)(t = 1.86,0.69,0.68 ,0.79,P > 0.05).Conclusion The results suggested that therapeutic efficacy of IFN-α-lb was not significantly different between B,C genotypes.
3.Changes in invariant nature kiler T (iNKT) cell percentages and subsets in immune organs of mice at different stages of obesity
Dongzhi CHEN ; Jingnan ZHANG ; Huijuan ZHAO ; Rui LIANG ; Jingfang TENG ; Xiang GAO ; Ming MENG
Chinese Journal of Microbiology and Immunology 2021;41(1):12-22
Objective:To observe the changes in percentages and subsets of invariant nature kiler T (iNKT) cells in adipose and related tissues at different stages of obesity, and analyze the role of iNKT cells during chronic inflammation in adipose tissues in a mouse model of obesity established with high-fat diet.Methods:Changes in mouse body weight, mental state, glucose tolerance and insulin tolerance were recorded. Hematoxylin and eosin (HE) staining was used to observe pathological changes in adipose tissues. Flow cytometry was performed to detect the percentages and subsets of iNKT cells as well as the percentages and subtypes of macrophages. The levels of cytokines in serum samples and the culture supernatants of lymphocytes in adipose tissues were detected with CBA. The expression of related proteins in adipose tissues was detected by Western blot.Results:(1) The volume of adipose cells increased significantly after four weeks of high-fat feeding, but the infiltration of inflammatory cells was not obvious. Significantly increased infiltration of inflammatory cells was observed after 12 weeks of high-fat feeding. (2) High-fat feeding could reduce the percentage of iNKT cells, increase the proportion of iNKT1 subgroup and decrease the proportion of iNKT10 subgroup in adipose tissues. The proportion of iNKT1 subgroup in thymus increased, but that of iNKT2 subgroup decreased. The percentage of macrophages and the proportion of M1 subgroup in adipose tissues increased, while the proportion of M2 subgroup decreased, which were more obvious after 12 weeks of high-fat feeding. (3) High-fat feeding resulted in decreased expression of E4BP4 and arginase-1 (Arg-1) in adipose tissues and increased expression of inducible nitric oxide synthase (iNOS). (4) High-fat feeding significantly increased the pro-inflammatory cytokines and decreased the anti-inflammatory cytokines in mouse serum and culture supernatants of lymphocytes in adipose tissues with more significant changes observed after 12 weeks of high-fat feeding.Conclusions:Increased iNKT1 and decreased iNKT10 in obese adipose tissues might be closely related to the increased M1 polarization and the imbalance of iNKT subsets might be involved in the progression of chronic inflammation in obese adipose tissues.
4.Regulation of intercellular adhesion molecule-1 expression in murine glomerular mesangial cells by lipoprotein(a)
Wei XIANG ; Xiaojie HE ; Zhuwen YI ; Jingnan HE ; Xiaochuan WU ; Shengmiao FU ; Huineng XI ; Chi CHENG ; Fuli WANG
Journal of Chinese Physician 2008;10(5):603-606
Objective To investigate the effects of Lp(a)on proliferation GMCs of rat model induced by lipopolysaccharide and explore the possible mechanism of Lp(a)in the proliferation of rat GMCs.Methods To observe the effects of Lp(a)on proliferation of GMCs,different dosage of Lp(a)were used,The research were divided into three groups:Control group,LPS group,Lp(a)group.After culture(at the end of 12h,24h,48h,60h and 72h),the cultured GMCs and suspension were collected to observe the rate of GMCs proliferation by MTT,the positive rate of proliferation cell nuclear antigen(PCNA)by immunohistochemisty,and the level of intercellular adhesion molecule-1(ICAM-1)by ELISA respectively.Results Compared with control and LPS group,MTT,positive rate of PCNA and ICAM-1 of GMCs were increased more significantly in Lp(a)group.MTT ,the positive rate of PCNA and ICAM-1 of GMCs were increased as Lp(a)dosage increased,a maximal effect was seen when Lp(a)was 2.5 μg/L or 5.0μg/L.When the dosage continue increased,MTT,the positive rate of PCNA and ICAM-1 activity of GMCs began to decrease in Lp(a)group.ICAM-1 showed positive correlation with MTT and the positive rate of PCNA.Conclusion Lp(a)can significantly affect the rate of GMCs proliferation,and this affection is in a dosage-and timedependent manner.Low dosage stimulates GMCs proliferation, and high dosage inhibits GMCs proliferation.ICAM-1 shows positive correlation with MTT and the positive rate of PCNA.The effect of Lp(a)on GMCs may be through ICAM-1.