1.A retrospective analysis on the incidence and treatment outcomes of retinopathy of prematurity among extremely preterm infants
Chaohui LIAN ; Guoming ZHANG ; Bingchun LIN ; Song TANG ; Peihui LIU ; Chuanzhong YANG
Chinese Pediatric Emergency Medicine 2015;22(7):491-493
Objective To analyze the incidence of retinopathy of prematurity(ROP)among extreme-ly preterm infants,and to evaluate the treatment methods and effects among those with severe ROP.Methods A retrospective analysis was performed to analyze incidence of ROP in 96 cases of extremely preterm infants who were born at a gestational age of 〈28 weeks and survived beyond a postmenstrual age of at least 1 year from Apr 2006 to Oct 2013,and to analyze the treatment outcomes of photocoagulation and ranibizum-ab intravitreal injection among the infants with severe ROP.Results Fifty-six of 96 cases(58.33%)grew into ROP finally and 21 cases(21.88%)grew into severe ROP,2 cases(2.08%)grew into aggressive poste-rior ROP.Fifteen cases with severe ROP were treated with laser photocoagulation.Four cases with severe ROP were received ranibizumab intravitreal injection prior to photocoagulation.Two cases with severe ROP were only treated with ranibizumab intravitreal injection.The eyesight of 96 patients (100%)in this study were all preserved.Conclusion ROP screening should focus on extremely preterm infants because of higher incidence of ROP and severe ROP among them.The infants with severe ROP should be treated with laser photocoagulation in time.The infants in critical condition or with aggressive posterior ROP can be treated with ranibizumab injection.
2.Astragaloside IV inhibits the development of heart failure in rats by regulating the nuclear factor E2-related factor 2/heme oxygenase-1 signaling pathway
Bingchun SONG ; Fanjing MENG ; Pei NIE ; Xiqing WEI ; Jinguo ZHANG
Chinese Journal of Geriatrics 2020;39(9):1072-1076
Objective:To investigate the effect of Astragaloside Ⅳ on abdominal aorta constriction-induced cardiac hypertrophy by activating the nuclear factor E2-related factor 2/heme oxygenase-1(Nrf2/ HO-1)signaling pathway, so as to improve cardiac function.Methods:From Sep.2017 to Jan.2019, 40 male SD rats were selected and abdominal aortic constriction(AAC)was used to establish a rat model of chronic heart failure.Rats were divided into three ACC groups: the model group, the benazepril HCl group and the Astragaloside Ⅳ group, plus the sham operation group.Rats in the benazepril HCl and Astragaloside Ⅳ groups were given 10 mg·kg -1·d -1 benazepril HCl and 50mg·kg -1·d -1 Astragaloside Ⅳ respectively by gavage, and the sham operation group and the model group were given normal saline of the same volume by gavage.After 8 weeks of treatment, cardiac structure and functional parameters were examined using cardiac color doppler ultrasound, while hemodynamics and morphological changes of myocardial cells were detected by immunofluorescence, serum brain natriuretic peptide(BNP)levels were detected by an enzyme-linked immunosorbent assay(ELISA), and Nrf2 and HO-1 mRNA expression in myocardial tissues were detected by reverse transcription-quantitative real-time PCR(RT-qPCR). Results:Compared with the sham operation group, the ratio of heart weight to femoral neck length(495.47±12.38), the ratio of heart weight to body weight(6.44±0.18), left ventricular end-diastolic diameter(LVEDD)(4.72±0.04 mm), left ventricular posterior wall thickness(LVPWT)(1.87±0.03)mm and the BNP level(151.61±5.67)mmol/L all increased( P<0.05), but the expression of mRNA Nrf2(0.36±0.02)and HO-1(0.27±0.02)decreased( P<0.01)in the model group.Compared with the model group, the ratio of heart weight to femoral neck length(261.88±12.97 and 286.40±12.56), the ratio of heart weight to body weight(3.38±0.13 and 3.71±0.15), left ventricular end-diastolic diameter(5.84±0.05)mm and (6.01±0.10)mm, left ventricular posterior wall thickness[(1.57±0.03)mm and(1.64±0.03)mm]and the BNP level[(99.40±4.97)mmol/L and(120.66±5.80)mmol/L]all decreased( P<0.05), but the mRNA expression of Nrf2(1.06±0.01 and 1.04±0.01)and HO-1(1.08±0.06 and 0.95±0.02)increased in the benazepril HCl and Astragaloside Ⅳ groups, respectively( P<0.01). Conclusions:Astragaloside Ⅳ has an effect of anti-oxidative stress, can inhibit heart failure and improve cardiac function, and its mechanisms may be related to the Nrf2/ HO-1 signaling pathway.
3.Differential effects of treadmill exercise on cyclooxygenase-2 in the rat hippocampus at early and chronic stages of diabetes.
Sung Min NAM ; Sun Shin YI ; Ki Yeon YOO ; Ok Kyu PARK ; Bingchun YAN ; Wook SONG ; Moo Ho WON ; Yeo Sung YOON ; Je Kyung SEONG
Laboratory Animal Research 2011;27(3):189-195
Cyclooxygenase-2 (COX-2) is believed to be a multifunctional neural modulator that affects synaptic plasticity in the hippocampus. In the present study, we investigated the differential effects of treadmill exercise on COX-2 immunoreactivity in the dentate gyrus in early and chronic diabetic stages in Zucker diabetic fatty (ZDF) rats and lean control (ZLC) rats. To this end, ZLC and ZDF rats at 6 or 23 weeks of age were put on a treadmill with or without running for 1 h/day for 5 consecutive days at 16-22 m/min for 5 weeks or 12-16 m/min for 7 weeks, respectively. Treadmill exercise in prediabetic and chronic diabetic rats significantly reduced blood glucose levels. In particular, exercise in the prediabetic rat blocked the onset of diabetes. COX-2 immunoreactivity was mainly detected in the granule cell layer of the dentate gyrus and stratum pyramidale of the CA3 region in all groups. COX-2 immunoreactivity was significantly increased in these regions of ZLC and ZDF rats after treadmill exercise in the early diabetic stage. However, COX-2 immunoreactivity was not changed in these regions in ZDF rats after treadmill exercise in the chronic stage. These results suggest that treadmill exercise in diabetic animals in the chronic stage has limited ability to cause plasticity in the dentate gyrus.
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Blood Glucose
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Cyclooxygenase 2
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Dentate Gyrus
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Hippocampus
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Plastics
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Rats
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Running
4.Mechanism of Astragalus methylside alleviating cardiomyocyte hypertrophy
Jiejie ZHANG ; Xiqing WEI ; Bingchun SONG ; Youqian LI ; Hongsheng ZHANG ; Zhencai GAO ; Cheng SHEN ; Jinguo ZHANG
Chinese Journal of Geriatrics 2022;41(7):837-842
Objective:To investigate the protective effects and related mechanisms of Astragaloside Ⅳ(ASⅣ)alleviating Angiotensin II-induced cardiomyocyte hypertrophy.Methods:H9c2 cardiomyocytes were divided into six groups: normal control group, ASⅣ group(ASⅣ 100 μmol/L), AngⅡ group(AngⅡ 1 μmol/L), and three ASⅣ dose experiments(AngⅡ 1 μmol/L + ASⅣ 25 μmol/l group, AngⅡ 1 μmol/L+ ASⅣ 50 μmol/l group, AngⅡ1 μmol/L+ ASⅣ 100 μmol/L group), and simultaneously cultured for 24 hours.Cardiomyocyte viability was assessed by CCK8 assay, and surface area of culturedcardiomyocytes in each group was assessed by immunofluorescence assay.Atrial natriuretic peptide(ANP)mRNA expression was assessed by fluorescence real-time quantitative RT-PCR.And LC3 protein expression, an autophagy related protein, was assessed by Western blotting as well as immunofluorescence.Results:(1)AngⅡ decreased cardiomyocyte H9c2 viability in a dose-dependent manner( P<0.05). ASⅣ could inhibit the decrease of cardiomyocyte H9c2 viability in response to AngⅡ in a dose-dependent manner( P<0.05). (2)H9c2 cardiomyocytes induced by AngⅡ showed a significantly larger cell area and significantly higher ANP mRNA and ANP protein expression compared with controls.Different concentrations of ASⅣ intervention could reverse the increase of cardiomyocyte H9c2 area induced by AngⅡ and also decreased the expression of ANP protein induced by AngⅡ in a dose-dependent manner(all P<0.05). (3)Compared with the control group, the autophagy level and the expression of autophagy marker LC3II/I of H9c2 cardiomyocytes induced by AngⅡ were significantly increased(all P<0.05). ASⅣ could inhibit AngⅡ-activated autophagy, and the difference was statistically significant( P<0.05). ASⅣ inhibited the expression of LC3II/I in H9c2 cardiomyocytes stimulated by AngⅡ, and the difference was statistically significant( P<0.05). Conclusions:ASⅣ inhibits AngⅡ-induced cardiac hypertrophy by inhibiting autophagy of cardiomyocytes.