Quercetin improves contrast-induced acute kidney injury through the HIF-1α/lncRNA NEAT1/HMGB1 pathway

ContextThe risk of contrast-induced acute kidney injury (CI-AKI) is increasing and the harm is great. Quercetin is the main active component in Abelmoschus manihot (L.) Medik (Malvaceae) and was reported to reduce the expression of HIF-1α.ObjectiveWe investigate whether quercetin improves the CI-AKI through the HIF-1α/lncRNA NEAT1/HMGB1 pathway.Materials and methodsHK-2 cells were treated with iohexol (200 mg/mL) for 6 h to establish a CI-AKI model. Quercetin (20 μM) was administered to CI-AKI cells cultured in dishes for 24 h. Cell morphology was observed by a fluorescence microscope. MTT and TUNEL assays were used to detect cell survival rate and apoptosis. Relative mRNA levels were measured by qRT-PCR. Protein levels were detected using western blotting. IL-6 and TNF-α protein levels were tested by Elisa assay. Targeting binding sites of HIF-1α and lncRNA NEAT1 were detected by luciferase assay.ResultsThe IC₅₀ value of quercetin was 163.25 μM. The expression levels of HIF-1α, lncRNA NEAT1 and HMGB1 were upregulated in the CI-AKI cell model. Quercetin diminished cell injury and apoptosis via inhibiting HIF-1α. Silencing of HIF-1α targeting lncRNA MEAT1 diminished cell injury and apoptosis. Silencing lncRNA NEAT1 has the same effect via suppressing HMGB1 expression. Collectively, quercetin diminished cell injury and apoptosis in CI-AKI cell model via the inhibition of HIF-1α on lncRNA NEAT1/HMGB1 signalling pathway.Discussion and conclusionsQuercetin diminished cell injury and apoptosis in CI-AKI cell mode via the inhibition of HIF-1α on the lncRNA NEAT1/HMGB1 signalling pathway, offering a potential novel therapeutic target for CI-AKI therapy.     

62例咽旁间隙肿瘤临床分析

目的：探讨咽旁间隙肿瘤的诊断和治疗方法及熟悉咽旁间隙解剖与肿瘤关系。方法：回顾性分析62例咽旁间隙肿瘤的临床资料。结果：咽旁间隙肿瘤中病理类型较多,但以神经鞘膜肿瘤比例较大,占41.9%,混合瘤22.6%,畸胎瘤、错构瘤、脊索瘤、恶性淋巴瘤及脑膜瘤等共占35.5%。进行以颈侧入路为主的4种手术入路,2例肿瘤复发（1例神经鞘膜瘤,1例转移癌）,再次手术治愈,其余均一次性手术治愈。结论：咽旁间隙肿瘤临床表现复杂,病理类型多样,肿瘤预后较好。其诊断较难,除症状体征外,CT、MRI及B超对咽旁间隙肿瘤的诊断有重要价值。手术径路是根据患者体征、影像学特征结合肿瘤位置、大小及性质而最终确定。颈侧入路为主要手术途径,气管切开为预防窒息措施。     

糖尿病肾病患者血浆硫醇氨基酸与中医辨证分型的相关性研究

目的:探讨与糖尿病肾病中医诊断相关的潜在生物标志物对于中医药现代化、客观化具有的重要意义.方法:应用高效液相色谱一三重四极杆质谱联用测定各证型DN患者和健康志愿者的血浆中8种硫醇氨基酸的含量,通过对照比较病例之间的差异.结果:DN患者体内Cys-gly和GSH的含量与健康人相比,显著降低;而SAH、SAM、Hey、Cysta和Cys含量随着病情的加重有逐渐增高的趋势.根据SAH和Hcy能明显区分气阴两虚偏阴虚与阴阳两虚组.另外,气阴两虚偏气虚组患者体内的SAH含量与阴阳两虚组相比也有显著性差异.结论:体内Cys-gly、GSH含量可辅助DN的早期中医诊断,体内SAH和Hcy的含量与DN各证型具有一定的相关性.     

救必应提取物心血管药理作用

研究表明:救必应醇提物具有降低冠脉流量、减慢心率及使心肌收缩力减弱,提高耐缺氧能力及抗心律失常作用;救必应水提物作用与醇提物相似,但减慢心率及减弱心肌收缩力的作用不明显。     

Antihyperglycemic sesquiterpenes from Psacalium decompositum.

Psacalium decompositum was investigated for antihyperglycemic compounds using diabetic ob/ob mice as a model for type 2 diabetes. In vivo bioassay-guided fractionation of an aqueous extract from the roots of P. decompositum led to the isolation of two new eremophilanolides, 3-hydroxycacalolide (1a) and epi-3-hydroxycacalolide (1b). A 1:1 mixture of 1a/1b exhibited antihyperglycemic activity when tested at 1.09 mmol/kg in ob/ob mice. The known furanoeremophilanes, cacalone (2a) and epicacalone (2b), were also isolated from the aqueous extract and were inactive. The known furanoeremophilane, cacalol (3), was isolated from a CH2Cl2 extract of P. decompositum roots and possessed antihyperglycemic activity. The relative stereochemistry in 1a and 1b was assigned 3R,5S and 3S,5S, respectively, based on ROESY data, 3J H-H values, and molecular mechanics calculations. Complete 13C and 1H NMR chemical shifts were assigned for 1a, 1b, 2a, 2b, and 3, and several revisions in 13C NMR assignments for 2a and 3 were made. Results from the conformational analysis of 1a, 1b, 2a, and 2b indicate that each compound exists in one major conformation in solution with H3-12 in a pseudoaxial position.     

Louki Zupa decoction attenuates the airway inflammation in acute asthma mice induced by ovalbumin through IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway

ContextAsthma is a common respiratory system disease. Louki Zupa decoction (LKZP), a traditional Chinese medicine, presents a promising efficacy against lung diseases.ObjectiveTo investigate the pathogenic mechanism of asthma and reveal the intervention mechanism of LKZP.Materials and methodsForty-eight female Balb/c mice were randomly divided into 6 groups: normal control group (NC), ovalbumin (OVA)/saline asthma model group, OVA/LL group, OVA/LM group, OVA/LH group and OVA/DEX group (n = 8 per group). The asthmatic mice were modelled through intraperitoneal injecting and neutralizing OVA. LKZP decoction was administrated by gavage at the challenge stage for seven consecutive days (2.1, 4.2 and 8.4 g/kg/day). We investigated the change in lung function, airway inflammation, mucus secretion and TH-1/TH-2-related cytokines. We further verify the activated status of the IL-33/ST2/NF-κB/GSK3β/mTOR signalling pathway.ResultsLKZP was proved to improve asthmatic symptoms, as evidenced by the down-regulated airway resistance by 36%, 58% and 53% (p < 0.01, p < 0.001 vs. OVA/saline group), up-regulated lung compliance by 102%, 114% and 111%, decreased airway inflammation and mucus secretion by 33%, 40% and 33% (p < 0.001 vs. OVA/saline group). Moreover, the content of cytokines in BALF related to airway allergy (such as IgE) and T helper 1/T helper 2 cells (like IL-2, IL-4, IL-5, IL-13, TNF-α and IFN-γ), were also markedly reduced by 13–65% on LKZP intervention groups compared with model group. Mechanistic research revealed that the IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway was activated in the OVA/saline group and LKZP significantly down-regulated this pathway.Discussion and conclusionLKZP improves lung function, airway inflammation, mucus secretion and correct immune imbalance by intervening with the IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway, presenting a promising therapeutic choice for asthma.     

眼铁质沉着症的临床分析

目的:探讨眼铁质沉着症(ocular siderosis)的临床特点及治疗方案。方法:对我院2002年1月至2006年12月收治的64例眼铁沉着症患者进行回顾性分析。结果:56例手术取出残留的异物,其中33例异物最大长径≤2.0mm,位于下方睫状体扁平部或锯齿缘附近26例;眼眶X光正侧位照片联合薄骨位照片异物显影阳性率76.56%,超声生物显微镜(Ultrasound biomicroscope,UBM)异物显影阳性率47.62%;晶状体前囊铁锈沉着发生率100%,继发性青光眼发生率7.69%,视网膜脱离发生率13.84%;视网膜电流图(Electroretino-gram,ERG)karpe分期Ⅲ期占7/10和Ⅳ期占3/10;56例患者作了眼内异物取出,异物取出率100%,术中发现16.07%病例异物磁性消失。结论:眼铁质沉着症残留的异物以最大长径≤2.0mm为主,主要位于下方睫状体扁平部或锯齿缘附近;眼眶X光照片为首选的检查方法,UBM可作为眼前段异物影像学检查辅助手段;ERG改变以karpe分期的Ⅲ期和Ⅳ期为主;玻璃体手术是取出眼内异物最有效的治疗手段。眼科学报2007;23:231-237.     

CYP1A1 and CYP1B1 genetic polymorphisms and uterine leiomyoma risk in Chinese women

Purpose  The aim of the study was to evaluate the association of CYP1A1 and CYP1B1 polymorphisms with uterine leiomyoma in Chinese women. Methods  We investigated 100 women with clinically diagnosed uterine leiomyoma and 110 healthy normal subjects from Chinese women. The genetic distribution of two CYP1A1 polymorphisms at MspI, Ile462Val and four CYP1B1 polymorphisms at Arg48Gly, Ala119Ser, Leu432Val, Asp449Asp were analyzed by polymerase chain reaction–restriction fragment length polymorphism and DNA sequencing method. Results  All the SNPs showed polymorphisms in Chinese women. The genotype A/G and the allele G on Ile462Val was significantly different between uterine leiomyoma patients and controls (P < 0.05). Conclusion  These results suggest that the genotype of CYP1A1 Ile462Val was associated with the increased risk of uterine leiomyomas in Chinese women. Capsule This is the first report that demonstrates the polymorphism at Ile462Val of CYP1A1 to be associated with uterine leiomyoma in Chinese women.     

Activation of phospholipase D involved in both injury and survival in A549 alveolar epithelial cells exposed to H2O2

To determine the role of the phospholipase D (PLD) pathway in injury and survival of alveolar epithelial cells, A549 cells were exposed to H₂O₂ (500 μM) which resulted in time-dependent injury and bi-phasic increase of PLD activity at 5 min and at 3 h, respectively. n-Butanol (0.5%) inhibited PLD activation, attenuated cell injury at 5 min of H₂O₂ exposure, but enhanced injury at 3 h of exposure. This activation was inhibited by treatment with catalase (500 units/ml). Exogenous phosphatidic acid mimicked the effects of PLD activation, and diphenyliodonium (NADPH oxidase inhibitor) reversed the decline in cell viability induced by H₂O₂ exposure. Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H₂O₂-induced PLD activation but reversed H₂O₂-induced injury. We speculate that PLD activation at the initiation of H₂O₂ exposure predominantly results in NAPDH oxidase activation, which mediates A549 cell injury, but turns to mediating cell survival as the H₂O₂ attack continues, which might be mainly due to the accumulation of intracellular phosphatidic acid.