根际低氧胁迫下外源亚精胺对黄瓜幼苗多胺和抗氧化系统的影响

采用营养液水培,研究了根际低氧胁迫下不同浓度外源亚精胺（Spd）处理对黄瓜幼苗根系和叶片中多胺含量、抗氧化酶活性、O₂^ˉ 产生速率、H₂O₂和MDA含量的影响。结果表明,营养液中添加0.05 mm ol·L^-1 Spd,可促进低氧胁迫下黄瓜幼苗的生长,缓解低氧胁迫的伤害;低氧胁迫下黄瓜幼苗体内抗氧化酶活性和多胺含量之间存在着密切的关系,0.05 mmol·L^-1外源Spd可明显提高植株体内Spd和Spm含量,降低Put含量,提高（Spd + Spm）/ Put比值,增强抗氧化酶活性,降低O₂^ˉ 产生速率、H₂O₂和MDA含量,从而促进植株的生长,提高植株对低氧胁迫的耐性。     

根际低氧对不同抗性猕猴桃幼苗抗氧化系统的影响

 【目的】研究低氧胁迫下,猕猴桃苗期体内活性氧代谢及抗性与抗氧化系统间的内在联系。【方法】用水培通氮气低氧胁迫法,研究低氧胁迫对‘秦美’猕猴桃（抗低氧型）和‘红阳’猕猴桃（低氧敏感型）两种抗性不同的猕猴桃实生苗抗氧化系统的影响。【结果】随胁迫时间的延长,两种猕猴桃叶、根内超氧化物歧化酶（SOD）、过氧化物酶（POD）和过氧化氢酶（CAT）活性增强, 超氧阴离子自由基（ ）、过氧化氢（H2O2）、丙二醛（MDA）含量增加;质膜透性（RPMP）增大,耐低氧的‘秦美’猕猴桃活性氧增加速度明显低于‘红阳’猕猴桃,抗氧化酶活性增加幅度明显高于‘红阳’猕猴桃;相同胁迫下,同种猕猴桃叶和根内抗氧化酶活性最大值出现的时间和增加幅度不同。【结论】抗低氧能力强的猕猴桃有较强的抗氧化保护系统;叶和根对低氧胁迫的感受和适应机理不同。     

低氧–复氧对脊尾白虾呼吸代谢和抗氧化酶活力的影响

以静室呼吸耗氧–复氧为实验组,持续充气组为对照组。于0、1、2、4、5 h及复氧1、4、8 h检测并分析了水体溶解氧(DO)和脊尾白虾(Exopalaemon carinicauda)组织主要呼吸代谢及抗氧化酶活力。结果显示,随着时间的延长,实验组DO不断降低,且显著低于对照组(P<0.05)。脊尾白虾鳃、肝胰腺和肌肉细胞色素C氧化酶(CCO)、琥珀酸脱氢酶(SDH)活力降低;乳酸脱氢酶(LDH)、延胡索酸还原酶(FRD)活力升高,SDH/FRD值降低。复氧后,3种组织SDH、LDH和FRD活力恢复至对照组,肌肉CCO活力升高,在复氧8 h时低于对照组(P<0.05);SDH/FRD值升高。随着时间的延长,3种组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPX)和谷胱甘肽S转移酶(GST)活力均先升后降,但肝胰腺的过氧化物酶(POD)活力降低,而在鳃和肌肉中呈波动性变化;复氧后,3种组织SOD、CAT、GPX和GST活力均恢复至对照组水平,但鳃和肌肉的POD在复氧8 h时均低于对照组(P<0.05)。研究表明,随着DO的降低,脊尾白虾有氧代谢逐渐降低,无氧代谢逐渐升高。复氧后,有氧代谢能力又逐渐恢复。上述抗氧化酶可能在脊尾白虾应对低氧-复氧中产生的氧化损伤发挥着重要作用。     

miR-323 regulates hypoxia-induced apoptosis of H9C2 cardiomyocytes through FGF9

AIM: To investigate the effect of microRNA-323 (miR-323) on the apoptosis of hypoxia-induced rat H9C2 cardiomyocytes and its mechanism. METHODS: The hypoxic injury model was established in the H9C2 cells. Anti-miR-323, pcDNA-FGF9 and si-FGF9 were transfected into the H9C2 cells and cultured under hypoxic condition for 48 h. The expression of miR-323 was detected by qPCR. The protein levels of fibroblast growth factor 9 (FGF9), cleaved caspase-3, c-Jun N-terminal kinase (JNK) and p-JNK were determined by Western blot. The cell viability was measured by MTT assay, and the apoptosis was analyzed by flow cytometry. The method of bioinformatics was applied to predict the target gene of miR-323, and dual-luciferase reporter assay was used for further validation. RESULTS: Hypoxia greatly reduced the viability of H9C2 cells at 12 h, 24 h and 48 h (P<0.05), and remarkably increased apoptotic rate and the protein level of cleaved caspase-3 in a time-dependent manner (P<0.05). The expression of miR-323 and the protein level of p-JNK were up-regulated and the expression of FGF9 was down-regulated in the H9C2 cells exposed to hypoxia (P<0.05). Down-regulation of miR-323 and over-expression of FGF9 obviously increased the viability of the H9C2 cells exposed to hypoxia, and decreased the apoptotic rate and the protein level of cleaved caspase-3 (P<0.05). FGF9 was the target gene of miR-323. Down-regulation of FGF9 reversed the attenuating effect of down-regulation of miR-323 on hypoxia-induced H9C2 cell injury. miR-323 regulated FGF9 and affected p-JNK level. CONCLUSION: miR-323 affects the viability and apoptosis of H9C2 cardiomyocytes under hypoxia by targeting FGF9 and regulating JNK signaling pathway.     

Injury pathways of hypoxia/reoxygenation in AC16 cardiomyocyte

AIM:To investigate the effects of hypoxia/reoxygenation (H/R) for different reoxygenation times on cardiomyocyte injury. METHODS:Human cardiomyocyte AC16 was cultured in glucose-free and serum-free DMEM with 1% O₂ for 24 h, 10% fetal bovine serum and low glucose DMEM combined with 21% O₂ were used to establish reoxygenation for 2 h, 6 h and 12 h, respectively. The cell viability was measured by CCK-8 assay. The protein levels of different cell injury pathway related molecules, such as LC3-Ⅱ/-I (autophagy), caspase-1 and gasdermin D (pyroptosis) and caspase-3 and Bax/Bcl2 (apoptosis), were determined by Western blot. RESULTS:Compared with blank control group, the cell viability in each H/R group was continuously decreased with the extension of reoxygenation time (P<0.05). The expression of LC3-Ⅱ/-I was up-regulated in hypoxia group and H/R group compared with blank control group (P<0.05). In addition, the protein levels of cleaved caspase-1 and cleaved gasdermin D were increased in H/R groups for 6 h and 12 h, respectively (P<0.05). Cleaved caspase-3 and Bax/Bcl2 were increased after reoxygenation for 12 h (P<0.05). CONCLUSION:Autophagy in hypoxia-induced AC16 cells is up-regulated, and then decreased by reoxygenation. The cell pyroptosis is activated earlier than the apoptosis during reoxygenation.     

Liver disease in dogs with tracheal collapse

BACKGROUND: Hepatopathy in dogs with chronic respiratory diseases is poorly recognized. The aim of this study was to evaluate liver parameters alanine transferase, alkaline phosphatase, and glutamate dehydrogenase, as well as basal and stimulated bile acid concentration, in dogs with tracheal collapse. HYPOTHESIS: Dogs with tracheal collapse have hepatopathy. ANIMALS: 26 dogs with tracheal collapse. MATERIALS AND METHODS: Gall bladder contraction was stimulated by intramuscular injection of a synthetic cholecystokinin analogue (ceruletide). Twelve healthy Beagle dogs and 30 dogs of various breeds investigated previously without evidence of hepatic, gastrointestinal, or respiratory diseases served as control. Amelioration of liver variables was assessed after stent implantation. RESULTS: Twelve of 26 (46%) dogs had increased serum activity of 2 or more liver enzymes. Serum basal bile acid concentrations were high in 24 of 26 dogs. Twenty- and 40-minute stimulated bile acids were significantly higher in dogs with tracheal collapse (64.2 +130.0/-43.0 micromol/L and 82.6 +164.0/-57.1 micromol/L) compared to the control dogs (7.0 +/- 3.6 micromol/L and 6.4 +/- 3.5 micromol/L). All twelve dogs reevaluated after a median of 58 days (48-219 days) had a normal breathing pattern and significantly decreased 20 and 40 minutes stimulated bile acids (50.0 +92.7/-32.8 micromol/L, 52.8 +97.6/-34.3 micromol/L; P = .0043), whereas plasma liver enzyme activities were not significantly influenced. CONCLUSION AND CLINICAL IMPORTANCE: There was a significant hepatic dysfunction in the majority of dogs with a tracheal collapse. Liver function should be routinely assessed in dogs with severe respiratory disease.     

小鼠实验性缺氧脑和肺组织MDA·LD含量和LDH活性变化

[目的]探讨小鼠实验性缺氧脑和肺组织丙二醛、乳酸含量和乳酸脱氢酶活性变化。[方法]将18只小鼠随机分为3组:正常对照组、急性缺氧组、急性一氧化碳染毒组,测定脑和肺组织MDA、LD含量、LDH活性。[结果]急性缺氧组和急性一氧化碳染毒组小鼠脑和肺组织MDA和LD含量显著增高。与对照组相比,急性缺氧组和急性一氧化碳染毒组小鼠肺组织中LDH活性显著降低,而在脑组织无显著性变化。MDA和LD含量在缺氧早期,脑和肺组织是易变化性指标,其改变可能与该组织损伤程度有关。LDH变化说明肺组织比脑组织对缺氧产生的自由基损伤更敏感。[结论]该模型为畜牧生产和水产养殖中出现的机体缺氧提供理论依据和实践指导。     

高原鼢鼠对低氧环境适应的生理指标研究进展

高原鼢鼠是终生生活于封闭洞道中的地下鼠,其洞道内氧浓度低,并且随着季节、土质、土壤含水量和洞道深度而发生波动。为了探讨高原鼢鼠对低氧环境的适应机制,通过对其机体调节氧转运有关的生理指标变化进行研究,综述了高原鼢鼠适应低氧环境的研究进展。     

HIF-2α在高原动物低氧适应中的研究进展

近年来,全基因组扫描和候选基因分析结果都表明低氧诱导因子调控的信号通路相关基因在藏族群体得到高表达。初步揭示了高原动物对高原低氧环境的适应机制,并发现了一系列对藏族人群适应高原低氧环境发挥作用的候选基因。其中低氧诱导因子-2α(HIF-2α)基因在低氧诱导通路中起着最关键作用,加深对HIF-2α的研究有助于进一步认识藏族人群低氧适应的机制。文中对HIF-2α的结构,分布,表达及调控进行了系统的阐释,并着重对HIF-2α在高原人群中的研究进展进行讨论,还对今后的研究发展方向进行了展望。     

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