Xu Y.,Hebei University |
Niu P.,Hebei University |
Zhang L.,Hebei University |
Du N.,BaoDing Women and Childrens Health Hospital |
And 2 more authors.
Proceedings - 2010 3rd International Conference on Biomedical Engineering and Informatics, BMEI 2010 | Year: 2010
Purpose: to study the anti-tumor effect and corresponding mechanism of Xinghuayu injection. Methods: (1) anti-tumor effect: Kunming mice were inoculated with hepatoma H 22 cells, and then were divided into model group, three dose Xinghuayu injection group and positive group, drug administrate red intraperitoneally once a day. After 7 days, the mice were killed to strip out the tumor blocks to weight. (2) synergistic action: take tumor-inoculated mice and divide them into Xinghuayu injection group, cyclophosphamide group and Xinghuayu combined cyclophosphamide group. All administration and other process was the same as that in (1). (3) measurement of serum IL-2 and TNF-α: take tumor-inoculated mice and divide them into model group, three dose Xinghuayu group and cyclophosphamide group. Administration to the above groups was the same as in (1). Take blood and detect the concentration of serum IL-2 and TNF-α. Results: (1) the tumor block weight of every Xinghuayu injection group is lower than model group, P < 0.01. (2) the tumor block weight of drug combination group is significantly lower than that of either single drug group, and the tumor inhibition ratio is significantly larger than either single drug group, P<0.05. (3) both of the serum IL-2 and TNF-α concentrations in middle and high dose Xinghuayu group are significantly larger than that of model group, P<0.01. Conclusion: Xinghuayu injection can inhibit tumor cell growth in tumor-bearing mice, and can enhance the anti-tumor effect of cyclophosphamide; Xinghuayu can increase the serum IL-2 and TNF-αconcentration in tumor-bearing mice, suggesting that Xinghuayu's anti-tumor effect is related with enhanced immune function. ©2010 IEEE.
Liu F.,Hebei Medical University |
Liu G.-J.,Hebei Medical University |
Liu N.,Peoples Hospital of Dingzhou |
Zhang G.,Peoples Hospital of Dingzhou |
And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2015
Hydrogen sulfide (H2S) is believed to be involved in numerous physiological and pathophysiological processes, and now it is recognized as the third endogenous signaling gasotransmitter, following nitric oxide and carbon monoxide; however, the effects of H2S on inflammatory factors in acute myocardial ischemia injury in rats have not been clarified. In the present study, sodium hydrosulfide (NaHS) was used as the H2S donor. Thirty six male Sprague Dawley rats were randomly divided into five groups: Sham, ischemia, isch¬emia + low dose (0.78 mg/kg) NaHS, ischemia + medium dose (1.56 mg/kg) NaHS, ischemia + high dose (3.12 mg/kg) NaHS and ischemia + propargylglycine (PPG) (30 mg/kg). The rats in each group were sacrificed 6 h after the surgery for sample collection. Compared with the ischemia group, the cardiac damage in the rats in the ischemia + NaHS groups was significantly reduced, particularly in the high dose group; in the ischemia + PPG group, the myocardial injury was aggravated compared with that in the ischemia group. Compared with the ischemia group, the levels of interleukin (IL) 1β, IL 6 and tumor necrosis factor α (TNF α) in the serum of rats in the ischemia + medium and high dose NaHS groups were significantly reduced, and the expression of inter-cellular adhesion molecule 1 (ICAM 1) mRNA and nuclear factor κ light chain enhancer of activated B cells (NF κB) protein in the myocardial tissues of rats was significantly reduced. In the ischemia + PPG group, the TNF α, IL 1β and IL 6 levels in the serum were significantly increased, the expression of ICAM 1 mRNA was increased, although without a significant difference, and the expression of NF κB was increased. The findings of the present study provide novel evidence for the dual effects of H2S on acute myocardial isch¬emia injury via the modulation of inflammatory factors. © 2015, Spandidos Publications. All rights reserved.
Yan X.Y.,First Hospital of Baoding |
Yan X.Y.,Peoples Hospital of Dingzhou |
Cheng Z.Y.,First Hospital of Baoding |
Cheng Z.Y.,Peoples Hospital of Dingzhou |
And 12 more authors.
Chinese Journal of Cancer Biotherapy | Year: 2011
Objective: To investigate the effect of phosphatase and tensin hemology deleted on chromosome ten gene (PTEN) on proliferation, apoptosis, VEGF (vascular endothelial growth factor) and its receptor VEGFR1 expression in human umbilical vein endothelial cell (HUVEC) line ECV304. Methods: Recombinant adenovirus containing green fluorescent protein (GFP) and PTEN (Ad PTEN GFP) or empty vector (Ad GFP) were transfected into ECV304 cells; proliferation and apoptosis of ECV304 cells were measured by MTT assay, Hoechst3342 staining and flow cytometry, respectively; PTEN, VEGF, VEGFR1 mRNA expression levels in Ad PTEN GFP transfected ECV304 cells were examined by quantitative PCR; and VEGF protein level in ECV304 cell supernatant was detected by ELISA. Chick chorioallantoic membrane (CAM) assay was used to study the effect of PTEN on angiogenesis. Results: Ad PTEN GFP transfection significantly inhibited the proliferation and induced apoptosis of ECV304 cells and the inhibitory rate and apoptotic rate were (50.38±5.42)% and (73.3±5.3)% at 5 d. VEGF and VEGFR1 mRNA expression levels were (13.40±1.32)% and (46.12±5.20)% of untransfected group after transfected with Ad PTEN GFP at MOI=100 in ECV304 cells. Furthermore, CAM assay results showed that Ad PTEN GFP transfection inhibited CAM angiogenesis in vivo. Conclusion: PTEN can inhibit the growth of and promote apoptosis of human umbilical vein endothelial ECV304 cells, which might be related to the down regulation of VEGF/VEGFR1 expression and the resulting angiogenesis inhibition.