1.Inhibition of laser-induced choroidal neovascularization by anti-osteopontin antibody
Yan, SU ; Peipei, ZHANG ; Fang, LIU
Chinese Journal of Experimental Ophthalmology 2014;32(9):813-818
Background It has been proved that as an important adhesion protein of extracellular matrix,osteopontion (OPN) can affect tumor neovascularization.Some new researches showed that anti-OPN antibody plays a role in regulating the neovascular vessel formation.Choroidal neovascularization (CNV) has the same structure with tumor neovascularization,but whether anti-OPN antibody restricts new vessel formation is unclear.Objective This study was to investigate the inhibitory effect of anti-OPN antibody on CNV.Methods Laser-induced CNV models were created in 40 eyes of 40 male SPF C57BL/6J mice by Argon laser photocoagulation of retinas,with the wavelength 514 nm.Thirty-six successful models were randomly divided into anti-OPN antibody group,mouse-IgG group and PBS group by the randomized number table.On the second day after photocoagulation,anti-OPN antibody of 400 μg was intraperitoneally injected in the anti-OPN antibody group,and the equivalent amount of mouse IgG and PBS were used in the same way in the mouse IgG group and PBS group.The CNV was evaluated by fundus fluorescein angiography (FFA) on the seventh days after photocoagulation.The mice were immediately sacrificed and the eyeballs were enucleated on the fourteenth day after photocoagulation,and 4 eyeballs in each group were used to observe the areas of CNV on the retinal pigmental epithelium-choroid-sclera fiat mounts,and the other 8 eyeballs of each groups were used to analyze the expression levels of OPN mRNA and vascular endothelial growth factor(VEGF) mRNA using quantitative fluorescence-PCR (QF-PCR).Results FFA showed fluorescein leakage areas around laser spots 7 days after photocoagulation,indicating that CNV appeared.The CNV areas were ([16.98±0.70] × 103) μm2,([27.13 ± 0.81] × 103) μm2 and ([35.39±2.14] ×103) μm2 respectively in the anti-OPN antibody group,mouse IgG group and PBS group,with a significant difference among the 3 groups (F =533.76,P =0.00),and the CNV area was significantly smaller in the anti-OPN antibody group compared with those of the mouse IgG group and PBS group (q =-3.95,-4.40,both at P<0.05).No significant difference was found in the OPN mRNA expression between the antiOPN antibody group and mouse IgG group (t =-5.26,P =0.66).However,the expression of VEGF mRNA in choroidal tissue was significantly declined in the anti-OPN antibody group than that in the mouse IgG group (t =-6.74,P<0.01).Conclusions Anti-OPN antibody suppresses the formation of CNV in laser-induced mouse model by down-regulating VEGF.
2.Effect of propofol pretreatment on cytokines and protection of renal ischemia/reperfusion injury in rats
Su LIU ; Zhenqiang FANG ; Genf ZHANG
Journal of Third Military Medical University 2003;0(17):-
Objective To explore the effect of propofol on tumor necrosis factor-alpha(TNF-?),interleukin-6(IL-6),interleukin-8(IL-8)in rats following renal ischemia/reperfusion and the protection of propofol on renal ischemia-reperfusion injury.Methods Seventy-two adult SD rats were randomly divided into three groups:sham operation group,ischemia/reperfusion group(I/R group)and propofol group(n=24 in each group).All the indexes of the last two groups were detected on 1,4 and 24 h after reperfusion.Five minutes before ischemia in propofol group,propofol was infused by vein and isometric physiologic saline to the other two groups.The concentration of IL-6,IL-8,TNF-? in serum and renal tissue,BUN and SCr in serum were measured.Hematoxylin and eosin staining for the renal tissue was processed.Results The concentration of IL-6,IL-8,TNF-? in serum and TNF-? in renal tissue in propofol group within 1 h after reperfusion was significantly lower than I/R group(P
3.Key Problems on Promoting University Students' Online Ideological and Political Work
Bu-Ping LIU ; Su-Fang HUANG ; Chun-Ping FANG ;
Chinese Journal of Medical Education Research 2006;0(10):-
From the development situation of chinese intemet and the need of college students' growth,this paper advanced six key problems on promoting university students' online ideological and political work.
4.Up-regulation of miR-22 through Wnt pathway suppresses proliferation, migration and invasion in human gastric MGC803 cells by DADS
Yunyun TANG ; Yi TANG ; Fang LIU ; Jian SU ; Hong XIA ; Bo SU ; Xi ZENG ; Qi SU
Chinese Pharmacological Bulletin 2017;33(8):1141-1147
Aim To investigate the up-regulation of miR-22 through Wnt pathway inhibits the proliferation,migration and invasion in human gastric MGC803 cells induced by diallyl disulfide(DADS).Methods The effects of proliferation,migration,and invasion of gastric cancer cells were evaluated by MTT,wound-healing and invasion assays.Online prediction software was applied to search the target gene of miR-22.Luciferase report gene assay was used to assess the target genes Wnt-1 of miR-22.The expressions of Wnt-1,β-catenin and TCF-4 were tested by qRT-PCR and Western blot,respectively.Results MTT showed that DADS and miR-22 notably decreased the proliferation compared with control group(P<0.05).Wound-healing assay showed that DADS and miR-22 could significantly inhibit the migration of MGC803 cells compared with the control group, especially in miR-22+DADS(P<0.05). Invasion assay showed that DADS and miR-22 could markedly inhibit the invasion of MGC803 cells compared with the control group, especially in miR-22+DADS(P<0.05). Online prediction software to search the target gene exhibited that Wnt-1 may be a target gene of miR-22. Luciferase report gene assay disclosed that Wnt-1 was identified as a direct target of miR-22. Qrt-PCR showed that the expression of Wnt-1 Mrna was respectively down-regulated by DADS and miR-22 compared withcontrol group, especially in miR-22+DADS(P<0.05). Western blot exhibited that DADS and miR-22 obviously suppressed the expressions of Wnt-1, β-catenin and TCF-4 proteins, especially in miR-22+DADS(P<0.05).Conclusion Up-regulation of miR-22 through Wnt pathway can remarkably suppress the proliferation, migration and invasion in MGC803 cells by DADS.
5.Protective effects of hyperbaric oxygen in secondary spinal cord injury
Fang LIU ; Hong CHEN ; Hua SU ; Jia CHEN
Chinese Journal of Physical Medicine and Rehabilitation 2010;32(9):649-652
Objective To investigate the mechanism underlying the protective effect of hyperbaric oxygen (HBO) in secondary spinal cord injury (SCI). Methods Models of acute SCI were established in 96 SpragueDawley rats using Allen's dropping weight technique. The rats were then divided into a HBO group, a high pressure nitrogen normal oxygen group, a normal pressure oxygen group and a normal pressure air group. The injured spinal cords were sampled for morphological studies at the 1 st, 3rd, 7th and 14th day after injury. Apoptotic cells were labeled using the TUNEL technique, and the expression of caspase-3 was detected. The neurological functionality of the spinal cord was assessed by open field locomotor evaluation ( the BBB score). Results The expression of caspase3 in the HBO group decreased significantly more than in the other groups after injury. The number of TUNEL-positive cells was significantly lower in the HBO group as well. Neurological function improved significantly after HBO therapy. Conclusions HBO can down-regulate the expression of caspase-3 and inhibit cell apoptosis in rats after SCI.The protective effect of HBO was related with the oxygen level.
7.Clinical efficacy of combination therapy with continuous intravenous pumping of Endostar and SOX regimen in advanced primary carcinoma of the liver
Jin SU ; Xinhua XU ; Kezhi SHI ; Fang YI ; Yang LIU
The Journal of Practical Medicine 2016;32(17):2908-2911
Objective To evaluate the efficacy and safety of combination therapy of Endostar and oxaliplatin plus S-1 ( SOX regimen) in patients with advanced Primary carcinoma of the liver. Methods 32 advanced primary liver cancer patients admitted from February 2012 to August 2014 were assigned to SOX regimen as systemic chemotherapy: oxaliplatin 130 mg/m2 iv d1; S-1 (80 ~ 120 mg, twice-daily) for 14 days; 150 mg Endostar which was dissolved in 210 mL normal saline for 120 h durative transfusion. Treatment was repeated every 21 days. Objective clinical efficacy and adverse effect was assessed every 2 cycles. Serum alpha fetoprotein (AFP) level was also monitored according to the schedule. Results All 32 patients were available to be assessed, the objective response rate (ORR), disease control rate (DCR) ,the clinical benefit response rates (CBR), 1 year survival rate was 15.6%, 46.9%, 56.3%, 58.3% respectively. The serum AFP respond rate was 19.4%. Major adverse effects were myelosuppression and fatigue , mostly graded at 1 ~ 2. There were no treatment-related death. Conclusions These preliminary results suggest that continuous intravenous pumping of Endostar combined with SOX regimen could provide survival benefits with tolerable adverse effects.
8.Blocking IL-17A protects against lung injury-induced pulmonary fibrosis through promoting the activation of p50NF-kappaB.
Su MI ; Zhe LI ; Hong LIU ; Zhuowei HU ; Fang HUA
Acta Pharmaceutica Sinica 2012;47(6):739-44
This study is to determine the preventive effect and mechanism of targeting IL-17A on pulmonary inflammation and fibrosis after acute lung injury. Mice were treated with anti-IL-17A antibody on the day 7 and sacrificed on the day 14 after bleomycin lung injury. The pulmonary inflammatory status and the deposition of collagen were measured by HE and Sirius stains staining. The contents of hydroxyproline and collagen were measured by using commercial kits. The survival rate of mice was calculated by Kaplan-Meier methods. The inflammatory cytokines in bronchoalveolar lavage fluid were measured by ELISA and the expressions of inflammation-related molecules were detected by Western blotting assay. Targeting of IL-17A could prevent the development of lung inflammation, decrease collagen deposition and the contents of hydroxyproline, and protect against the development of pulmonary fibrosis, which together led to an increase in the animal survival. Moreover, blocking IL-17A decreased the expression ofpro-fibrotic cytokines such as IL-17A, TGF-beta1 and IL-13; increased the expression of anti-fibrotic or anti-inflammatory factors such as IFN-gamma, COX-2, 5-LOX, 15-LOX. Indeed, IL-17A antagonism suppressed the activation of pro-inflammatory p65NF-kappaB but enhanced the activation of pro-resolving p50NF-kappaB. In conclusion, that blockade of IL-17A prevents the development of pulmonary fibrosis from acute lung injury, is because blocking IL-17A may prevent acute inflammation converting to chronic inflammation.
9.Change the Conception,Strengthen the Management
Zhimin LIU ; Na PU ; Yan SU ; Bing FANG ; Yuling XU
Journal of Kunming Medical University 2007;0(S2):-
Medical therapy,education and scientific research are three functions of a hospital,in which education is one of the core tasks.The author thinks that we should strengthen the cultivation of the teachers;raise the level of the managements;increase the teaching input and reinforce the reform of education and scientific research so as to drive and improve the development of the hospital.
10.The effects of different amounts of iodine intake on the immune status of patients with Graves disease
Junping SU ; Shengou SU ; Bo ZHANG ; Yunxia CHEN ; Chunyan LIU ; Shujun JI ; Xin YU ; Fang BIAN
Clinical Medicine of China 2012;28(1):44-46
ObjectiveTo investigate the effects of different amounts of iodine intake on the cellular and humoral immune in Grave's disease (GD) patients.MethodsThe clinical GD cases were diagnosed by thyroid fine needle Cytology examination.Patients in GD group are divided into GD group Ⅰ and GD group Ⅱ based on the median of urine iodine.The blood levels of FT4,FT3,TSH,TPOAb,TGAb,TRAb and TNF-t were detected.The difference and association of these parameters between these groups were analyzed.ResultsThe TNF-αt level in GD Ⅰ group was higher than that of GD Ⅱ group( P > 0.05 ) ;The average level of TRAb of GD Ⅰgroup ( [ 1.4 ±0.2 ] U/L) were higher than that of GD Ⅱ group ( [ 1.2 ± 0.1 ] U/L) ( P < 0.05 ) ;The positive rates of TGAb and TPOAb of GD Ⅰ group were higher than that of GD Ⅱ group ( P < 0.05 ).The percentages of patients with high level of TGAb and TPOAb in GD Ⅰ group ( 78.9% 、84.2% ) were higher than that in GD Ⅱ group (50.0%,62.5% ) ( x2 =6.79,10.70,P <0.05 ) ; Analysis showed a linear positive correlation of TNF-αwith TRAb and TPOAb ( r is 0.489 and 0.563,P < 0.01 ).ConclusionIodine is an important factor to the development of Graves disease.Excessive iodine intake will exaggerate the GD condition and patients with GD should be controlled for iodine intake.