人体成分分析仪指导营养治疗对妊娠期糖尿病的影响

目的观察人体成分分析仪指导营养治疗对妊娠期糖尿病患者疾病控制及母婴结局的影响。方法从2016年9月—2017年10月河北省人民医院收治的妊娠期糖尿病患者中选取124例作为研究对象,随机将其分为治疗组和对照组,每组各62例。对照组给予一般饮食指导及正常产检,治疗组依据人体成分分析结果进行营养治疗,同时建立个人行为追踪档案,定期干预。对比两组患者分娩方式、孕妇结局与围生儿结局。结果两组顺产率比较,差异有统计学意义(P<0.05),治疗组高于对照组。两组剖宫产率比较,差异有统计学意义(P<0.05),治疗组低于对照组;妊娠期高血压、糖尿病并发症、羊水过多、孕期感染比较,差异有统计学意义(P<0.05),治疗组低于对照组;两组围生儿巨大儿、新生儿窒息、围生儿死亡、转NICU比较,差异有统计学意义(P<0.05),治疗组低于对照组。结论人体成分分析仪指导营养治疗妊娠期糖尿病患者,可提高顺产率,降低剖宫产率,有效降低母婴并发症,改善母婴结局。

miR-138调控年龄相关性白内障晶状体上皮细胞抗氧化应激作用的机制

目的:探讨miR-138对年龄相关性白内障晶状体上皮细胞抗氧化应激能力的影响及其作用机制。方法:采用实时定量PCR(RT-q PCR)检测年龄相关性白内障与正常人透明晶状体前囊膜组织中及人晶状体上皮细胞系(SRA01/04)氧化应激模型中miR-138的表达水平。利用2',7'-二氯荧光黄双乙酸盐(DCFH-DA)荧光探针检测细胞内源性活性氧(reactive oxygen species,ROS)水平。向人晶状体上皮细胞中分别转染miR-138 mimics,mimic controls,miR-138 inhibitors,inhibitor controls 72h后细胞暴露于400μmol/L H_2O_2 1h,采用RT-qPCR检测p53和Bax的mRNA表达,western blotting检测p53和Bax的蛋白表达水平,MTS法检测细胞增殖活力。结果:与正常对照组相比,年龄相关性白内障晶状体组织中与人晶状体上皮细胞氧化应激模型中miR-138的表达均显著升高,差异有统计学意义(P<0.001);人晶状体上皮细胞氧化应激模型中内源性ROS的水平明显升高,差异有统计学意义(P<0.001)。相对于对照组,miR-138 mimics组p53和Bax的mRNA、蛋白表达水平均明显升高,细胞增殖活力明显下降,差异有统计学意义(均P<0.001);miR-138 inhibitors组p53和Bax的mRNA、蛋白表达水平均明显下降,细胞增殖活力显著升高,差异有统计学意义(均P<0.001)。结论:miR-138在年龄相关性白内障囊膜组织中表达上调,通过正调控下游靶基因p53和Bax,下调人晶状体上皮细胞抗氧化应激的能力,抑制人晶状体上皮细胞增殖和修复,从而参与年龄相关性白内障的发生过程。

miR-211 regulates the antioxidant function of lens epithelial cells affected by age-related cataracts

AIM： To investigate the effects and mechanism of miR-211 in mediating the antioxidant function of lens epithelial cells affected by age-related cataracts. METHODS： Real-time quantitative polymerase chain reaction （RT-qPCR） was used to detect miR-211 expression in the anterior lens capsules of healthy people, the anterior lens capsules of patients with age-related cataracts, and human epithelial cell line （SRA01/04） cells exposed to oxidative stress. A 2＇, 7＇-dichloro-fluorescein diacetate （DCFH-DA） probe was used to measure the levels of endogenous reactive oxygen species （ROS） in human lens epithelial cells （hLECs） exposed to 400 pmol/L H2O2 for lh. SRA01/04 cells were transfected with either miR-211 mimics, mimic controls, miR-211 inhibitors or inhibitor controls. After 72h, these cells were exposed to 400 IJmollL H2O2 for lh, then p53 and Bax mRNA expression were measured using RT-qPCR. p53 and Bax protein expression were also measured by Western blotting analysis. Finally, cell viability was assessed using an MTS assay. RESULTS： Compared to the control group, expression of miR-211 in the anterior lens capsules of age-related cataract patients and in SRA01/04 cells exposed to oxidative stress was significantly increased （P〈0.001）. Levels of endogenous ROS were significantly elevated in hLECs exposed to oxidative stress （P〈0.001）. Compared to the mimic control group, the hLECs in the miR-211 mimic group expressed significantly higher levels of p53 and Bax mRNA and protein while cell viability was significantly reduced （P〈0.001）. Conversely, p53 and Bax mRNA and protein expression were significantly reduced in the miR-211 inhibitor group as compared to the control group, while the cells in this group had much higher levels of call viability （P〈0.001）. CONCLUSION： miR-211 is upregulatsd in the anterior lens capsules of age-related cataract patients, miR-211 decreased the antioxidative stress capacity of lens epithelial cells by upregulating p53 and Bax, while inhibiting cell proliferation and repair. This finding suggests that miR-211 may play a key role in the development of age-related cataracts.

SUMOylation and deacetylation affect NF-κB p65 activity induced by high glucose in human lens epithelial cells

AIM: To explore the effects of IκBα SUMOylation and NF-κB p65 deacetylation on NF-κB p65 activity induced by high glucose in cultured human lens epithelial cells(HLECs).METHODS: HLECs(SRA01/04) were cultured with 5.5, 25, and 50 mmol/L glucose media for 24 h, and with 50 mmol/L glucose media for 0, 12, and 24 h respectively. SUMO1 and SIRT1 expressions were detected by reverse transcriptionpolymerase chain reaction(RT-PCR) and Western blot(WB). IκBα and NF-κB p65 expressions were detected by WB. With NAC, DTT, MG132 or Resveratrol(RSV) treatment, SUMO1 and SIRT1 expressions were detected by WB. Protein expression localizations were examined by immunofluorescence and co-immunofluorescence. The effects of SUMO1 or SIRT1 overexpression, as well as MG132 and RSV, on the nuclear expression and activity of IκBα and NF-κB p65 were analyzed by immunoblot and dual luciferase reporter gene assay.RESULTS: SUMO1 and SIRT1 expressions were influenced by high glucose in mRNA and protein levels, which could be blocked by NAC or DTT. SUMO1 was down-regulated by using MG132, and SIRT1 was up-regulated under RSV treatment. IκBα nuclear expression was attenuated and NF-κB p65 was opposite under high glucose, while IκBα and NF-κB p65 location was transferred to the nucleus. SUMO1 or SIRT1 overexpression and MG132 or RSV treatment affected the nuclear expression and activity of IκBα and NF-κB p65 under high glucose condition.CONCLUSION: IκBα SUMOylation and NF-κB p65 deacetylation affect NF-κB p65 activity in cultured HLECs under high glucose, and presumably play a significant role in controlling diabetic cataract.

miR-211 promotes lens epithelial cells apoptosis by targeting silent mating-type information regulation 2 homolog 1 in age-related cataracts

AIM： To detect the expression of miR-211 in age-related cataract tissue, explore the effects of miR-211 on lens epithelial cell proliferation and apoptosis, and identify its target gene.METHODS： This study used real-time quantitative polymerase chain reaction（RT-q PCR） to measure the expression of miR-211 and its predicted target gene [silent matingtype information regulation 2 homolog 1（SIRT1）] in 46 anterior lens capsules collected from age-related cataract patients. Human lens epithelial cell line（SRA01/04） cells were transfected with either miR-211 mimics, mimic controls, miR-211 inhibitors or inhibitor controls, 72 h after transfection, miR NA and protein expression of SIRT1 were measured using RT-qP CR and Western blotting; then cells were exposed to 200 μmol/L H2O2 for 1h, whereupon cell viability was measured by MTS assay, caspase-3 assay was performed. Dual luciferase reporter assay was performed to verify the relationship between miR-211 of SIRT1.RESULTS： Compared to the control group, expression of miR-211 was significantly increased（P〈0.001）, the miR NA and protein expression of SIRT1 were significantly decreased（P〈0.001） in the anterior lens capsules of patients with age-related cataracts. Relative to the control group, SIRT1 miR NA and protein levels in the miR-211 mimic group were significantly reduced, cell proliferation activity significantly decreased, and caspase-3 activity was significantly increased（P〈0.001）. In the miR-211 inhibitor group, SIRT1 miRNA and protein expression were significantly increased, cell proliferation activity significantly increased, and caspase-3 activity was significantly decreased（P〈0.001）. A dual luciferase reporter assay confirmed that SIRT1 is a direct target of miR-211.CONCLUSION： miR-211 is highly expressed in the anterior lens capsules of patients with age-related cataracts. By negatively regulating the expression of SIRT1, miR-211 promotes lens epithelial cell apoptosis and inhibits lens epithelial cell proliferation.

Regulation of Circadian Genes by the MAPK Pathway:Implications for Rapid Antidepressant Action

Accumulating evidence suggests that the circadian rhythm plays a critical role in mood regulation,and circadian disturbances are often found in patients with major depressive disorder(MDD).The mitogen-activated protein kinase(MAPK)/extracellular signal-regulated kinase(ERK)pathway is involved in mediating entrainment of the circadian system.Furthermore,the MAPK/ERK signaling pathway has been shown to be involved in the pathogenesis of MDD and the rapid onset of action of antidepressant therapies,both pharmaceutical and non-pharmaceutical.This review provides an overview of the involvement of the MAPK/ERK pathway in modulating the circadian system in the rapid action of antidepressant therapies.This pathway holds much promise for the development of novel,rapid-onset-of-action therapeutics for MDD.