One of the leading causes of diabetes-related deaths is myocardial damage, which may be the cause of heart failure in people with type 2 diabetes mellitus. The objective of the research was to look at the impact of coronary failure with kind a pair of type 2 diabetes mellitus. This project aimed to explore the protective impact of oleanolic acid on myocardial damage in type 2 diabetes mellitus and to investigate the connected mechanism. Specific pathogen free grade db/db male mice were elected as model, while the Db/m mice were opted for control. Different doses of drug intervention were performed and the general condition, cardiac function, blood glucose, blood lipids, degree of myocardial injury, and degree of oxidative stress were examined by morphological examination of myocardial tissues, biochemical examination, and gene and protein amount detection. The results showed that lactate dehydrogenase, creatine kinase isoenzyme, total cholesterol, triglycerides and malondialdehyde levels in serum of Db/db mice were increased, while phosphatidylinositol 3 kinase, protein kinase B, glucose transporter 4 expression and superoxide dismutase level in myocardial tissue were decreased. After using oleanolic acid, the serum concentrations of lactate dehydrogenase, creatine kinase isoenzyme, total cholesterol, triglycerides and malondialdehyde were declined in Db/db mice, while phosphatidylinositol 3 kinase, protein kinase B, glucose transporter 4 expression and superoxide dismutase level were rised. The results recommend that oleanolic acid has protective impact on cardiac muscle injury in Db/db mice and conjointly the mechanism could also be correlated with promoting the activation of phosphatidylinositol 3 kinase/protein kinase B/glucose transporter 4 signal transduction.

依据以创新能力培养为导向的教学理念,在教学过程中重点关注医学生创新能力的培养,尤其是终身自主学习能力、实践能力和科研素养.通过提升资源条件,构建以培养医学创新人才为导向的培养模式,探索以创新能力培养为导向的教学理念在医学教学中的应用.

目的 观察丁苯酞对弥漫性脑损伤大鼠咬合蛋白及基质金属蛋白酶(MMP)-9表达的影响.方法 240只成年SD大鼠随机数字法分为模型组(80只)、甘露醇组(80只)、丁苯酞+甘露醇组(80只),甘露醇组静滴甘露醇(剂量1.0 g/kg),丁苯酞+甘露醇组,在给予甘露醇的同时还要给予丁苯酞软胶囊灌胃(剂量0.4 ml/kg).每组分别在伤后3 h、12 h、24 h、72 h、144 h干湿法测定大鼠脑组织含水量、伊文思蓝法测定血脑屏障通透性、免疫组化和Werstern印迹测定咬合蛋白及MMP-9的表达变化.结果与模型组相比,甘露醇组在各时间点脑组织含水量明显减少(P<0.05),血脑屏障通透性明显降低(P<0.05),咬合蛋白及MMP-9的表达无明显差异(P>0.05).与甘露醇组相比,丁苯酞+甘露醇组各时间点脑组织含水量明显减少(P<0.05),血脑屏障通透性明显降低(P<0.05),咬合蛋白的表达明显增加(P<0.05),MMP-9的表达明显减少(P<0.05).结论 丁苯酞与甘露醇联合应用可明显减少弥漫性脑损伤大鼠脑水肿程度,改善血脑屏障通透性,增加咬合蛋白的表达,减少MMP-9的表达.

目的 探讨内皮素A受体拮抗剂BQ-123对蛛网膜下腔出血( SAH)大鼠学习记忆功能的改善作用及机制.方法 成年雄性SD大鼠随机分为Sham组、SAH组和BQ-123组;枕大池二次注血法建立SAH模型,BQ-123组经侧脑室注射BQ-123溶液给药剂量为18 μg;穿梭箱检测大鼠学习记忆功能;HE染色观察海马区神经细胞形态结构变化;免疫组织化学染色检测自噬相关因子Beclin-1和LC3-Ⅱ的表达水平.结果 与Sham组比较,SAH组学习记忆能力显著下降( P<0. 05),海马区神经细胞数量显著减少(P<0. 05),Beclin-1和LC3-Ⅱ的表达明显升高(P<0. 05);与SAH组相比,BQ-123组学习记忆能力得改明显改善(P<0. 05),海马区神经细胞丢失数量明显较少(P<0. 05),Beclin-1和LC3-Ⅱ的表达明显升高(P<0. 05).结论 BQ-123干预可减轻SAH损伤造成的学习记忆功能障碍,其机制与可能与调控海马区神经细胞自噬有关.

Almost all crops that are important to humans are sensitive to high salt concentration in the soil. The presence of salt in soil is one of the most significant abiotic stresses in farming. Therefore, improving plant salt tolerance and increasing the yield and quality of crops in salty land is vital. Transgenic technology is a fast and effective method to obtain salt-tolerant varieties. At present, many scholars have studied salt damage to plant and plant salt-tolerance mechanism. These scholars have cloned a number of salt-related genes and achieved high salt tolerance for transgenic plants, thereby showing attractive prospects. In this paper, the salt-tolerance mechanism of plants is described from four aspects: plant osmotic stress, ion toxicity, oxidative stress, and salt tolerance genes. This review may help in studies to reveal the mechanism of plant salt tolerance, screen high efficiency and quality salt tolerance crops.

Objective To investigate the effects of Edaravone on ERK1/2 protein and neuronal autophagy in rats with subarachnoid hemorrhage (subarachnoid hemorrhage,SAH).Methods 40 adult male rats (400 -450 g) were divided into four groups:sham operation (Sham),SAH model (The SAH model was replicated by intravascular puncture),Edaravone treament (5 mg/kg intraperitoneal injection modeling rats,repeat after 12 h) and ERK1/2 inhibitor (U0126) intervention (0.5 h prior to the modeling through the tail vein,0.05 mg/kg) groups by random number distribution method,for 10 rats in each group.After 24 h,the rats were executed and brains were taken,HE staining was used to observe the morphology and number of neurons in CA1 region of hippocampus;immunohistochemical staining was used to detect the Beclin-1,LC3-Ⅱ and p-ERK1/2 protein.Results Compared with the Sham group,the hippocampal neurons in the SAH group were disorganized,and the cells were mostly triangular pyramidal,and the number of surviving cells decreased significantly (P ＜0.05);the expression of Beclin-1 and LC3-Ⅱ was high (P ＜0.05);the expression of p-ERK1/2 was increased (P ＜0.05).Compared with the SAH group,the necrosis rate of nerve cells in Edaravone group decreased obviously,and the number of normal cells increased (P ＜0.05);the expression of Beclin-1 and LC3-Ⅱ increased significantly (P ＜0.05);the expression of p-ERK1/2 was increased significantly (P ＜0.05);Compared with the SAH group,the necrosis rate of nerve cells in U0126 group increased significantly,and the expression of Beclin-1 and LC3-Ⅱ decreased significantly (P ＜0.05);the expression of p-ERK1/2 decreased significantly (P ＜0.05).Conclusion Edaravone has neuroprotective effects on SAH,which may moderately increase autophagy levels mediated by the ERK1/2 signaling pathway,thereby reducing neuronal cell death.

Moderate hypothermia (MH) used as treatment for neurological diseases has a protective effect; however, its mechanism remains unclear. Neuronal autophagy is a fundamental pathological process of early brain injury in subarachnoid hemorrhage (SAH). We found that moderate activation of autophagy can reduce nerve cells damage. In this study, We found that MH can moderately increase the level of autophagy in nerve cells and improve the neurological function in rats. This type of autophagy activation is dependent on extracellular signal-regulated kinase (ERK) signaling pathways. The level of neuronal autophagy was down-regulated significantly by using U0126, an ERK signaling pathway inhibitor. In summary, these results suggest that MH can moderately activate neuronal autophagy through ERK signaling pathway, reduce nerve cell death, and produce neuroprotective effects.

目的 检测亚低温干预后蛛网膜下腔出血(SAH)大鼠神经细胞内质网应激及自噬的激活程度,探讨亚低温治疗的保护作用及机制.方法 将48只成年雄性SD大鼠随机分为假手术组(S组)、SAH组、全身亚低温组(H组)和内质网应激抑制剂组(TUDCA组).采用颈内动脉穿刺法建立大鼠SAH模型,H组于颈外动脉穿刺后即刻向大鼠全身喷洒乙醇进行体表降温,将直肠温度维持在30～32℃4 h;TUDCA组于颈动脉穿刺前1h腹腔注射溶于生理盐水(100 mg/mL)的牛磺熊去氧胆酸(TUDCA,内质网应激抑制剂)溶液,剂量4.5 mg/kg.术后24h取脑,HE染色法观察海马区神经细胞形态;免疫组织化学方法检测内质网应激相关因子GRP78、CHOP及自噬相关因子Beclin-1、LC3-Ⅱ的表达.结果 与S组相比,SAH组海马区存活神经细胞数量减少(P＜0.05),海马区GRP78、CHOP蛋白及Beclin-1、LC3-Ⅱ蛋白表达水平显著升高(P＜0.05).与SAH组相比,H组海马区存活神经细胞数量明显减少(P＜0.05),GRP78、CHOP及Beclin-1、LC3-Ⅱ蛋白表达水平显著升高(P＜0.05).与SAH组相比,TUDCA组海马区存活神经细胞数量明显减少(P＜0.05),GRP78、CHOP蛋白及Beclin-1、LC3-Ⅱ蛋白表达水平显著降低(P＜0.05).结论 亚低温可通过调控内质网应激激活神经细胞自噬,减轻蛛网膜下腔出血的早期脑损伤.

In this research, through the analyzing of the Triticum aestivum salt-tolerant mutant gene expression profile, under salt stress. A brand new gene with unknown functions induced by salt was cloned. The cloned gene was named Triticum aestivum salt stress protein (TaSST). GenBank accession number of TaSST is ACH97119. Quantitative polymerase chain reaction (qPCR) results exhibited that the expression TaSST was induced by salt, abscisic acid (ABA), and polyethylene glycol (PEG). TaSST could improve salt tolerance of Arabidopsis-overexpressed TaSST. After salt stress, physiological indexes of transgenic Arabidopsis were better compared with WT (wild-type) plants. TaSST was mainly located in the cytomembrane. qPCR analyzed the expression levels of nine tolerance-related genes of Arabidopsis in TaSST-overexpressing Arabidopsis. Results showed that the expression levels of SOS3, SOS2, KIN2, and COR15a significantly increased, whereas the expression of the five other genes showed no obvious change. OsI_01272, the homologous gene of TaSST in rice, was interfered using RNA interference (RNAi) technique. RNAi plants became more sensitive to salt than control plants. Thus, we speculate that TaSST can improve plant salt tolerance.

This study established a wheat transcriptome library using RH8706-49 and RH8706-34. Salt-induced differential genes were screened by Illumina RNA sequencing (RNA-Seq). Five differential genes were chosen to study the functions by combining transcript sequencing result and gene chip. The expression changes of these five differential genes were analyzed using real-time quantitative PCR (qRT-PCR) technique to determine the reliability and accuracy of transcriptome sequencing and transplanted into Arabidopsis thaliana to obtain transgenic homozygote plants for the salt tolerance test. The salt tolerance test results show that the transgenic plants grew far better than the wild-type plant.

The expression profile chip of the wheat salt-tolerant mutant RH8706-49 was investigated under salt stress in our laboratory. Results revealed a novel gene induced by salt stress with unknown functions. The gene was named as TaZNF (Triticum aestivum predicted Dof zinc finger protein) because it contains the zf-Dof superfamily and was deposited in GenBank (accession no. KF307327). Further analysis showed that TaZNF significantly improved the salt-tolerance of transgenic Arabidopsis. Various physiological indices of the transgenic plant were improved compared with those of the control after salt stress. Non-invasive micro-test (NMT) detection showed that the root tip of transgenic Arabidopsis significantly expressed Na(+) excretion. TaZNF is mainly localized in the nucleus and exhibited transcriptional activity. Hence, this protein was considered a transcription factor. The TaZNF upstream promoter was then cloned and was found to contain three salts, one jasmonic acid methyl ester (MeJA), and several ABA-responsive elements. The GUS staining and quantitative results of different tissues in the full-length promoter in the transgenic plants showed that the promoter was not tissue specific. The promoter activity in the root, leaf, and flower was enhanced after induction by salt stress. Moreover, GUS staining and quantitative measurement of GUS activity showed that the promoter sequence contained the positive regulatory element of salt and MeJA after their respective elements were mutated in the full-length promoter. RNA-Seq result showed that 2727 genes were differentially expressed; most of these genes were involved in the metabolic pathway and biosynthesis of secondary metabolite pathway.

A novel salt-induced gene with unknown functions was cloned through analysis of gene expression profile of a salt-tolerant wheat mutant RH8706-49 under salt stress. The gene was named Triticum aestivum salt-related protein (TaSP) and deposited in GenBank (Accession No. KF307326). Quantitative polymerase chain reaction (qPCR) results showed that TaSP expression was induced under salt, abscisic acid (ABA), and polyethylene glycol (PEG) stresses. Subcellular localization revealed that TaSP was mainly localized in cell membrane. Overexpression of TaSP in Arabidopsis could improve salt tolerance of 35S::TaSP transgenic Arabidopsis. 35S::TaSP transgenic Arabidopsis lines after salt stress presented better physiological indexes than the control group. In the non-invasive micro-test (NMT), an evident Na+ excretion was observed at the root tip of salt-stressed 35S::TaSP transgenic Arabidopsis. TaSP promoter was cloned, and its beta-glucuronidase (GUS) activities before and after ABA, salt, cold, heat, and salicylic acid (SA) stresses were determined. Full-length TaSP promoter contained ABA and salt response elements.

Based on microarray analysis results of the salt tolerant wheat mutant, we identified and cloned an unknown salt-induced gene Ta-UnP (Triticum aestivum unknown protein). Quantitative PCR results revealed that Ta-UnP expression was induced not only by salt but also by polyethylene glycol, abscisic acid, and other environmental stress factors. Under salt stress, transgenic Arabidopsis plants that overexpressed Ta-UnP showed superior physiological properties (content of proline, soluble sugar, MDA, and chlorophyll) compared with the control. Subcellular localization demonstrated that Ta-UnP was mainly localized on the cell membrane. The expressions of nine salt tolerance-related genes of Arabidopsis in Ta-UnP-overexpressed Arabidopsis were analyzed via OCR, and the results revealed that the expressions of SOS2, SOS3, RD29B, and P5CS were significantly up-regulated, whereas the other five genes only slightly changed. The results of the salt tolerance analysis indicated that Ta-UnP can enhance the salt tolerance of transgenic rice plants, and RNAi transgenic rice plants became highly susceptible to salt stress. The results from this study indicate that this novel Ta-UnP may be useful in improving of plant tolerance to salt stress. (C) 2014 Elsevier Inc. All rights reserved.