1.Effects of coal-burning type of fluorosis on hypothalamic-pituitary-ovary axis function in female rats
Xiuhui CHEN ; Shuhua XIA ; Siwen YU ; Jingfeng XU ; Maojuan YU ; Cheng WANG
Chinese Journal of Endemiology 2015;34(2):93-97
Objective To observe the influence of coal-burning type of fluorosis on hypothalamic-pituitaryovary axis function and to explore possible mechanism in female rats.Methods Sixty SD rats were divided into two groups according to body weight with the method of random number table:control group and fluorosis group,30 rats in each group.Fluorosis group was feed with corn powder baked by high fluorine coal from Zhijin area.Changes of female rats' teeth during fluorine exposure were observed.After feeding for 180 days,24 h urine was collected in estrus and fluorine level was tested using fluoride ion-selective electrode; rats were executed and bone fluorine level was tested with high-temperature ashing-fluorine ion-selective electrode.Femoral artery blood was collected and serum was separated to test the contents of follicle stimulating hormone (FSH),luteinizing hormone (LH),testosterone (T),estradiol (E2) and progesterone (P) with electrochemiluminescence radioimmunoassay and gonadotropin-releasing hormone (GnRH),inhibin (INH) with enzyme-linked immunosorbent assay (ELISA),respectively.Organs,including hypothalamus,pituitary gland and ovary were weighted,and organ coefficients were calculated.Pathological morphology of hypothalamus,pituitary gland and ovary was observed after staining and ultrastructure of ovary was examined by electron microscopy.Results Coal-burning induced fluorine poisoning rat model was established successfully.There were no significant differences statistically in organ coefficients between fluorosis groups (0.032 ± 0.004,0.014 ± 0.008,0.037 ± 0.009) and controls (0.035 ± 0.005,0.012 ± 0.006,0.035 ± 0.004,t =0.46,0.87,0.64,all P > 0.05).Rats serum GnRH,FSH,LH and T levels [(21.654 ± 4.765),(29.580 ± 5.221),(53.988 ± 6.506),(23.962 ± 2.255)μg/L] of fluorosis groups were all higher than those of controls [(10.384 ±2.250),(19.217 ± 4.743),(30.314 ± 4.443),(7.883 ± 1.973)μg/L,t =6.762,4.646,9.503,16.971,all P < 0.05].But the level of P,INH [(12.635 ± 3.841),(18.926 ± 3.465)μg/L] were all lower than those of controls [(21.045 ±4.768),(48.076 ± 3.525)μg/L,t =4.344,18.649,all P < 0.05].Serum E2 levels of control group and fluorosis group were (35.375 ± 10.662) and (27.500 ± 12.783)μg/L,respectively.The difference between groups was not statistically significant (t =1.821,P > 0.05).No pathological changes were observed in the two groups of female hypothalamus,pituitary tissue by light microscopy and electron microscopy.Under light microscope,in the control group of normal ovarian tissue,more corpus luteum and different developmental stages of follicles were seen,granulosa cells were neatly arranged in a monolayer or multilayer.In fluorosis group,severe edema of ovarian interstitial cells and follicle degeneration increased.Cell structure and cell contours were blurred and unclear with occasional mature follicles.Under transmission electron microscope,in control group,normal ovarian granulosa cell ultrastructure was observed,nuclei were round,nuclear chromatin was uniform distributed,cytoplasm was rich in mitochondria and endoplasmic reticulum,and normal morphology.In fluorosis group,granulosa cells and interstitial cells showed apoptotic characters,such as nucleoli disappearing,mitochondrial swelling and chromatin aggregating at the nuclear membrane.Conclusions Fluorosis can induce ovarian tissue apoptosis,severely damage the micro environment.Reduction of P and INH affects ovarian,maturation and ovulation and leads to secretion of GnRH,FSH and LH.Fluorosis caused by coal-burning may induce the injury of ovary and cause abnormal secretion of hypothalamic-pituitary-ovary axis.Fluorosis has affected parts of female axis which may not be in the hypothalamus,pituitary,but causes ovarian tissue damage.
2.Effect of overexpression of vascular cell adhesion molecule-1 on migration of murine mesenchymal stem cells
Yan CHENG ; Heng ZHU ; Yuanlin LIU ; Yanguo WANG ; Yue ZHAO ; Xiuhui CHEN ; Zhenlin YANG ; Yi ZHANG
Chinese Journal of Pharmacology and Toxicology 2016;(1):68-73
OBJECTIVE To investigate the effect of overexpression of vascular cell adhesion molecule-1(VCAM-1)on the migration in vitro of the murine mesenchymal stem cells(MSCs)and its possible mechanism. METHODS The migration ability of normal mouse MSC (C3) ,empty vector-transfected MSC(C3+N) and VCAM-1 transfected MSC(C3+VCAM-1)was assessed by Transwell culture system in vitro after incubation for 8 and 12 h,respectively. The fetal bovine serum (FBS) was used as the chemotactic agent to induce MSC migration. The transmigrated cells were detected with methylosaniliam chloride(crystal violet)as well as DAPI staining.Furthermore,the specific chemical inhibitors of mitogen-activation protein kinase (MAPK) pathway ( SB203580,PD98059 and JNK inhibitorⅡ)were added to the Transwell system for 12 h and the alteration of the MSC migration ability was evaluated. RESULTS After incubation with FBS for 8 and 12 h,the absolute migrated cell number(7467 ± 485 and 8795 ± 255)and migration rate〔(14.9 ± 1.0)% and(17.6 ± 0.5)%〕of MSC in C3+VCAM-1 group were significantly increased compared with C3 group〔2731±562 and 4779±224, (5.5 ± 1.1)%and(9.6 ± 0.4)%〕and C3+N group〔2539 ± 321 and 5645 ± 1080,(5.1 ± 0.6)%and(11.3 ± 1.1)%〕(P<0.05,P<0.01),but there was no significant difference between C3 and C3+N groups. Moreover,the MSC migration ability of C3+VCAM-1 group was partially suppressed by addition of JNK inhibitorⅡ. The transmigrated cell number(4843 ± 167)and migration rate〔(9.7 ± 0.3)%〕were decreased compared with those of C3+VCAM-1 group without JNK inhibitorⅡ(P<0.01). SB203580 and PD98059,as specific chemical inhibitors of MAPK pathway,had no effect on MSC migration. CONCLUSION VCAM-1 can enhance mouse MSC migration in vitro and th4e mechanism may be related to JNK/MAPK pathway activation.
3.Study on serum S100A12 level in patients with obstructive sleep apnea hypopnea syndrome
Peng ZHANG ; Xiuhui CHENG ; Hua ZHANG ; Songyun OUYANG ; Wenlong LI ; Linqing GUO ; Chao XU ; Yuna ZU ; Yongxin WU
Chongqing Medicine 2017;46(34):4780-4782
Objective To investigate the correlation and significance of S100A12 with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods Fifty-three patients with OSAHS were chosen as OSAHS group and 46 healthy volunteers were chosen as control group.The levels of S100A12 and hs-CRP in the two groups were compared,and its relationship with those of epworth (ESS),apnea hypopnea index (AHI),and minimum blood oxygen saturation (L-SpO2) were analysised.Results The scores of ESS,BMI,A HI,L-SpO2,hs-CRP and S100A12 in two groups were statistically significant (P<0.05).The severity of hs-CRP in severe OSAHS group was significantly higher than that of mild OSAHS group (P<0.05).There was no significant difference in hs-CRP between moderate OSAHS group and mild OSAHS group and severe group (P>0.05).The level of S100A12 in severe OSAHS group was significantly higher than that of moderate OSAHS group and OSAHS mild group(P<0.05).The level of S100A12 in moderate moderate group was significantly higher than that of mild group(P<0.01).hs-CRP was negatively correlated with ESS and AHI (r=0.822,0.787,P<0.01),was positively correlated with L-SpO2 (r=-0.740,P<0.01),S100A12 was positively correlated with ESS and AHI (r =0.707,P < 0.01),and negatively correlated with ESS and AHI (r =0.707,0.807,P<0.01),and negatively correlated with with L-SpO2 (r=-0.670,P<0.01).Conclusion S100A12 is associated with OSAHS.The higher the severity of OSAHS,the higher the S100A12 value,which can be used as a new predictor of cardiovascular disease risk in OSAHS patients.
4.Guidance for the clinical evaluation of traditional Chinese medicine-induced liver injuryIssued by China Food and Drug Administration.
Xiaohe XIAO ; Jianyuan TANG ; Yimin MAO ; Xiuhui LI ; Jiabo WANG ; Chenghai LIU ; Kewei SUN ; Yong'an YE ; Zhengsheng ZOU ; Cheng PENG ; Ling YANG ; Yuming GUO ; Zhaofang BAI ; Tingting HE ; Jing JING ; Fengyi LI ; Na AN
Acta Pharmaceutica Sinica B 2019;9(3):648-658