Background This study aimed to establish a novel, clinically translatable model of hypoxic preconditioning, termed intermittent hypoxic preconditioning (IHPC), to enhance acute hypoxic resistance in mouse hippocampal neurons. Methods Mice were allocated into three experimental groups: normoxic control, acute hypoxic exposure, and IHPC. The neuroprotective efficacy of IHPC was evaluated by neurological behavioral assessments, along with histological and molecular examinations of hippocampal neuronal viability and apoptosis. Results Behavioral analyses showed that while acute hypoxia significantly compromised cognitive function and neurological performance (both p < 0.05), IHPC pretreatment substantially ameliorated these deficits. At the molecular level, the IHPC group showed marked downregulation of the pro-apoptotic gene Bax and concomitant upregulation of the anti-apoptotic gene Bcl-2 compared with the acute hypoxia group. Consistently, compared with the acute hypoxia group, the IHPC group protein levels of cleaved caspase-3, caspase-8, and caspase-9 were significantly suppressed. TdT-mediated dUTP Nick-End Labeling (TUNEL) staining further corroborated these findings, compared with the acute hypoxia group, showing a substantial reduction in DNA fragmentation and staining intensity in the IHPC group, which indicated attenuated apoptotic activity. Conclusion This study shows that IHPC serves as an effective hypoxic preconditioning paradigm, conferring neuroprotection against an acute hypoxic insult by enhancing neuronal survival and suppressing apoptotic pathways in the hippocampal region.

Stroke is a serious threat to human health and current clinical therapies remain unsatisfactory. Elevated expression of Na+-K+-2Cl- cotransporter 1 (NKCC1) following stroke can disrupt the blood-brain barrier (BBB) and result in brain edema, indicating that NKCC1 may be a potential therapeutic target for improving stroke outcomes. Polygalasaponin F (PGSF) is a triterpenoid saponin isolated from Polygala japonica Houtt, which has showed neuroprotective effects in previous studies. The present study aimed to assess the protective effects of PGSF on cerebral ischemia-reperfusion injury (CIRI) in vivo and elucidate its underlying mechanism by targeting NKCC1. Experimental results revealed that following CIRI, rats displayed neurological deficits, cerebral infarction and brain edema, concurrent with increased NKCC1 mRNA and protein expression in the cerebral tissue. Notably, the administration of PGSF at both 10 mg/kg and 20 mg/kg effectively mitigated these adverse outcomes. To explore the mechanism of PGSF, pyrosequencing was used to find that CIRI reduces the methylation of the NKCC1 promoter, while PGSF enhances it. It was thereby demonstrated that PGSF could reduce NKCC1 expression in this manner. Simultaneously, we also observed that the protein expression of DNA methyltransferase 1 (DNMT1) in the ischemic penumbra was augmented after CIRI, whereas PGSF reduced the expression of DNMT1, which was contrary to the trend of NKCC1 methylation under the treatment of PGSF. These results imply that the enhancement of NKCC1 methylation by PGSF may not be catalyzed by DNMT1 and that the reduction of NKCC1 methylation level after CIRI may not be related to DNMT1. Finally, we discovered that PGSF can decrease the leakage of the BBB and enhance the expression of the BBB structural proteins occludin and ZO-1. In conclusion, PGSF can target NKCC1 as an epigenetic target and downregulate its expression following CIRI by enhancing DNA methylation of NKCC1, thereby safeguarding the structure and function of brain tissue.

Stroke is the second leading cause of mortality and the leading cause of adult disability worldwide. Neuroinflammation is a crucial mechanism that regulates the pathogenesis and prognosis of stroke and involves both peripheral and intracerebral immune cells. Neutrophils and microglia are the primary immune cells that mediate neuroinflammation and play bidirectional roles after stroke. Significant interactions between neutrophils and microglia exist. Microglia regulate the activation, infiltration, as well as formation of neutrophil extracellular traps (NETs), whereas neutrophils regulate the polarization and phagocytic activity of microglia. In this review, we summarize the bidirectional roles of neutrophils and microglia in stroke with an emphasis on the interactions between neutrophils and microglia, as well as the associated signaling pathways and targets involved. We further introduce potential stroke treatment drugs that regulate the interactions between neutrophils and microglia, including anti-inflammatory drugs and natural products. We propose that, according to the different ischemic times and cell activation states, regulating the interactions between neutrophils and microglia through relevant targets and signaling pathways may be an ideal strategy for the anti-inflammatory treatment of stroke, potentially improving treatment and prognosis of stroke.

It is widespread of endemic fluorosis in China, and the exposure of excessive fluoride will cause nervous system disease and activate microglia. However, the mechanism of the damage is not clear. It is well-known that NLRP3/Caspase-1/GSDMD pathway, a classic pyroptosis pathway, is widely involved in the occurrence and development of nervous system–related diseases, infectious diseases, and atherosclerotic diseases. This research aimed to explore the molecular mechanism of sodium fluoride on inflammation and pyroptosis in BV2 microglia based on the NLRP3/Caspase-1/GSDMD signaling pathway. BV2 microglia was treated with sodium fluoride at the dose of 0.25, 1, and 2 mmol/L for 24, 48, and 72 h, respectively. Cell viability, cell morphology, lactate dehydrogenase content, and related proteins and genes were examined to investigate if sodium fluoride caused damage to BV2 microglia through the pyroptosis pathway. Dithiolam (5 μmol/L), a pyroptosis inhibitor, was added for further verification. NaF could induced BV2 cells injury in a dose-dependent fashion through disrupting the integrity of cell membranes and increasing IL-1β via upregulating NLRP3, Caspase-1, and its downstream protein GSDMD. Disulfiram could improve these changes caused by NaF. In conclusion, our results suggested that NLRP3/Caspase-1/GSDMD-mediated classical pyroptosis pathway was involved in fluoride-induced BV2 microglia damage.

随着"脑卒中高危人群筛查和干预项目"的实施,脑卒中发病率已由2005年222/10万下降至2019年201/10万,但脑卒中仍是我国成人致死、致残的首位病因,具有高发病率、高致残率、高病死率、高复发率、高经济负担五大特点,其中缺血性脑卒中(ischemic stroke,IS)的发病率最高[1].越来越多的证据表明,炎性反应是脑卒中的重要诱发因素之一,过度的炎性反应会导致组织损伤.脑卒中发生后,小胶质细胞和星形胶质细胞作为疾病主要的效应细胞数小时内被激活,释放大量炎性因子白细胞介素(IL)-1β、IL-6、IL-8、TNF-α等,炎性因子诱导多种炎性细胞(中性粒细胞、单核细胞、巨噬细胞、不同亚型T细胞和其他炎性细胞)进入缺血区域,诱导产生大量趋化因子和其他因子触发一系列级联反应,加剧炎性反应,使缺血区域无法有效地恢复血流灌注,对神经系统造成不可逆的损伤.

目的:应用网络药理学及分子对接方法分析蒙药嘎日迪-13 治疗脑卒中的作用机制.方法:应用TCMSP数据库中各成分口服生物利用度及类药性筛选活性成分,并根据血脑屏障通透性进一步筛选治疗中枢神经系统疾病的活性成分,通过DisGeNET数据库预测嘎日迪-13 治疗脑卒中的潜在靶点;对靶点进行基因本体(gene Ontology,GO)、京都基因与基因组百科全书(kyoto Encyclopedia of Genes and Genomes,KEGG)和蛋白-蛋白相互作用(protein-protein interaction,PPI)分析,筛选关键靶点;应用分子对接验证化合物与关键靶点的结合能力.结果:通过TCMSP数据库筛选得到嘎日迪-13 的活性成分58 个,获得蒙药嘎日迪-13 治疗脑卒中潜在靶点 114 个;网络分析结果显示,嘎日迪-13 通过参与核因子κB(nuclear factor kappa-B,NF-κB)信号通路、白介素 17(interleukin 17,IL17)信号通路、低氧诱导因子-1(hypoxia induc-ible factor-1,HIF-1)信号通路等 27 条通路发挥保护作用,确定关键靶点包括:NOS3、ACE、IL6、TNF、SERPINE1、VEGFA、IL1 β、MMP9、CXCL8、TP53 以及MAPK1.结论:本研究通过网络药理学及分子对接提供了蒙药嘎日迪-13 治疗脑卒中的潜在分子依据,揭示了蒙药嘎日迪-13 治疗脑卒中的作用机制,为后续研究及临床应用提供了理论支持.

目的:探讨临床医生与基础教师联席授课的生理学案例教学法在医学生"早临床"实践中的意义.方法:以2019级麻醉班和法医班为观察组,2019级影像医学和精神医学班为对照组,在二年级上学期由临床医生和基础教师联席授课,采用翻转课堂模式进行生理学案例教学尝试,通过问卷调查评价教学效果.结果:绝大部分观察组学生认为在医学基础课程学习阶段就较早地采用此种由临床医生亲自指导去接触临床案例的教学方法,可以加强对理论知识的应用和自主学习能力的培养、从而更早地培养临床思维.学生参与愿意高,对这种授课模式持积极肯定态度.与对照组相比,更多观察组学生愿意按时完成课程学习,喜欢拓展阅读和讨论题形式的教学资源,表明观察组学生的学习积极性更高,对学习的广度和深度有更高的要求.更多观察组学生喜欢借助积极提问和交流完成课程学习,而且对自我学习管理能力的认可程度也较高.结论:临床医生与基础教师联席授课的生理学案例教学模式在激发学生学习兴趣、提高学生的学习和交流能力、培养学生的临床思维等方面发挥了积极的作用,为今后在临床医学专业推广生理学的"早临床"教学提供了参考模式.

目的:基于GEO数据库挖掘脑缺血再灌注损伤(Cerebral ischemia-reperfusion inju-ry,CIRI)中的关键靶点,并通过分子对接探讨瓜子金皂苷己(Polygalasaponin F,PGSF)抗CIRI的作用机制.方法:选择GEO数据库中CIRI芯片,应用R语言分析芯片的矩阵文件,筛选表达差异靶点,对结果进行可视化处理;将差异显著的靶点进行蛋白-蛋白相互作用分析,构建网络并根据拓扑参数筛选关键靶点.采用AutoDock Tools软件对PGSF与上述关键靶点进行分子对接,计算结合能.结果:通过GEO数据库筛选出CIRI差异表达靶点137个,在蛋白-蛋白相互作用网络中筛选得到关键靶点为:白细胞介素6(Interleukin-6,IL-6)、基质金属蛋白酶9(Ma-trix Metallopeptidase 9,MMP9)、CC型趋化因子配体2(C-C motif chemokine 2,CCL2)、细胞间黏附分子1(Intercellular adhesion molecule,ICAM1)和前列腺素G/H合酶2(Prostaglandin G/H synthase 2,PTGS2),PGSF与关键靶点对接得分为:-8.8、-7.3、-8.9、-7.9、-9.4 Kj/mol,说明PGSF可能与关键靶点结合,且具有较强的亲和力.结论:PGSF抗CIRI的作用机制可能与调控IL-6、MMP9、CCL2、ICAM1和PTGS2发挥抗炎、抑制血脑屏障破坏和减轻脑水肿有关.

目的:探讨基于优慕课的混合式教学模式在医学生理学教学中的应用效果.方法:选择2020级运动康复专业(39人)和临床医学专业(222人)的学生作为研究对象,在生理学的授课中采用基于问题为导向的教学法(PBL)+合作学习+翻转课堂+过程性评价的混合式教学模式,在学期末进行问卷调查.结果:绝大多数学生都喜欢生理学的学习;大部分学生通过一个学期的学习适应了这种教学模式,只有1.53％(4/261)的学生不喜欢这种模式;98.85％(258/261)的学生认为生理学的学习有助于其他课程的学习;95.40％(12/261)的学生认为通过这学期生理学的学习对于他们思考问题的方式产生影响,培养了用医学思维思考问题的能力,93.10％(243/261)的学生认为通过这种授课方式锻炼了他们的表达沟通能力,94.25％(246/261)的学生认为可以帮助他们加强合作交流,96.93％(253/261)的学生认为自主学习的能力有所提升;调查也显示,75.10％(196/261)的学生还是喜欢传统的授课方式;大部分学生都不喜欢在课堂上进行交流、回答问题等,而比较喜欢课下进行课后练习[53.64％(140/261)]、完成章节总结[40.23％(105/261)]或课前对上节课学过的内容进行小测试[50.19％(131/261)]的方式.结论:时代的发展使学习方式发生变化,通过混合式教学可以提高学生的自主学习能力,有助于培养学生用医学思维思考问题的能力,同时通过这种授课方式可以锻炼学生的表达沟通能力,加强学生的合作交流能力.

目的 探讨caspase在氟化钠(NaF)致心肌细胞凋亡中的作用.方法 将H9c2 心肌细胞分别暴露于含终浓度为 0(对照)、40 mg/L NaF以及 40 mg/L NaF+50 μmol/L Z-VAD-FMK的高糖培养基中 24、48、72 h.采用CCK-8 法检测细胞活性;采用倒置荧光显微镜观察细胞形态,并用TUNEL法观察细胞凋亡情况;通过qRT-PCR法检测心肌细胞Fas、caspase-1、caspase-8 及caspase-3 mRNA的表达情况;采用Western blot法检测心肌细胞中Fas、caspase-1、caspase-8 及caspase-3蛋白的表达情况.结果 与对照组相比,40 mg/L NaF染毒 24、48、72 h后,H9c2 心肌细胞的存活率均降低,差异有统计学意义(P＜0.05);与NaF组相比,NaF+Z-VAD-FMK组处理 24、48、72 h后,H9c2 心肌细胞的存活率均增加,差异有统计学意义(P＜0.05).与对照组相比,NaF组H9c2 心肌细胞的凋亡率增加,差异有统计学意义(P＜0.05);与NaF组相比,NaF+Z-VAD-FMK组H9c2 心肌细胞的凋亡率降低,差异有统计学意义(P＜0.05).与对照组相比,NaF组H9c2 心肌细胞Fas、caspase-8、caspase-1、caspase-3 mRNA和蛋白的表达水平增加,差异均有统计学意义(P＜0.05);与NaF组相比,NaF+Z-VAD-FMK组H9c2 心肌细胞Fas、caspase-8、caspase-1、caspase-3 mRNA和蛋白的表达水平降低,差异均有统计学意义(P＜0.05).结论 caspase通路及Fas介导的死亡受体通路可能参与氟化钠诱导的心肌细胞凋亡.

目的:观察瓜子金皂苷己(Polygalasaponin F,PGSF)是否影响氧糖剥夺/复氧(Oxygen and glucose deprivation/reoxygenation,OGD/R)处理的BV-2小胶质细胞炎性细胞因子及细胞因子信号抑制因子3(Suppressors of cytokine signaling3,SOCS3)表达,初步探讨PGSF对抗OGD/R炎症反应的机制.方法:构建BV-2小胶质细胞OGD/R体外模型,分为正常对照组、模型组、PGSF低剂量组、PGSF中剂量组及PGSF高剂量组.BV-2细胞氧糖剥夺2 h、复糖复氧6 h后提取总RNA,通过实时荧光定量多聚酶链式反应检测BV-2细胞炎性因子TNF-α、IL-1β、IL-6以及SOCS3的基因表达.结果:I/R后BV-2细胞中炎性因子TNF-α、IL-1β、IL-6及SOCS3的mRNA表达明显增加;给予PGSF处理可以逆转上述观察指标的改变.结论:PGSF在体外实验中具有抑制神经炎症的作用,SOCS3信号通路可能参与介导了PGSF的抗炎作用.

目的:采用大鼠脑缺血再灌注损伤模型观察瓜子金皂苷己(Polygalasaponin F,PGSF)对脑组织中钠-钾-氯协同转运蛋白1(Na+-K+-2Cl-combined transporter type 1,NKCC1)及炎症因子表达水平的影响.方法:将大鼠按体重随机分为假手术组、模型组、PGSF低剂量组、PGSF中剂量组、PGSF高剂量组,以线栓法制备大脑中动脉阻塞(Middle cerebral artery occlusion,MCAO)模型.除假手术组外其余各组缺血1 h、再灌注24 h.侧脑室立体定位注射给药.以实时荧光定量多聚酶链式反应检测肿瘤坏死因子α(Tumor necrosis factor,TNF-α)、白细胞介素1β(Interleukin-1β,IL-1β)、白细胞介素6(Interleukin-6,IL-6)及NKCC1的mRNA表达情况.结果:脑缺血再灌注处理使病灶组织中TNF-α、IL-1β、IL-6及NKCC1的mRNA表达量均较假手术组明显升高;与模型组相比,PGSF高剂量组、中剂量组及低剂量组TNF-α、IL-1β、IL-6的mRNA表达均明显下调,PGSF高剂量组和中剂量组NKCC1的mRNA表达也显著下调.结论:结合前期研究结果,推测NKCC1可能是PGSF在整体水平影响脑缺血再灌注损伤的重要靶点之一,PGSF还可能通过抑制炎症发挥作用.神经炎症可能直接或间接通过与NKCC1相关机制参与了脑缺血再灌注损伤的病理过程.

目的 研究氟化钠(sodium fluoride,NaF)是否通过Fas介导的死亡受体通路导致心肌细胞凋亡,探讨氟中毒致心肌损伤可能的作用机制.方法 用0.24、0.48、0.96 mmol·L-1 NaF处理H9c2心肌细胞,以制备NaF染毒细胞模型,以不加NaF的组作为对照组.通过CCK-8法检测细胞活力变化,用TUNEL法观察心肌细胞形态和凋亡情况,用Real-time PCR和Western blot方法检测心肌细胞中凋亡相关因子的mRNA和蛋白表达水平.结果 NaF可抑制H9c2细胞增殖,改变细胞形态,诱导细胞凋亡,且与染毒剂量及染毒时间有关.与对照组相比,NaF处理H9c2细胞24、48、72 h后,随NaF浓度的增加,Fas、caspase-1、caspase-8、caspase-3 mR-NA表达水平明显增加.染毒48 h后,随NaF浓度的增加,H9c2细胞Fas、caspase-1、caspase-8、cleaved caspase-3蛋白表达水平明显上调,明显高于对照组.结论 NaF可能通过Fas介导的死亡受体通路影响与凋亡相关的基因与蛋白的表达,导致心肌细胞凋亡,进而造成心肌细胞损伤.

Hemorrhagic transformation (HT) is a frequent complication of ischemic stroke after thrombolytic therapy and seriously affects the prognosis of stroke. Due to the limited therapeutic window and hemorrhagic complications, tissue plasminogen activator (t-PA) is underutilized in acute ischemic stroke. Currently, there are no clinically effective drugs to decrease the incidence of t-PA-induced HT. Hypoxia-inducible factor 1 (HIF-1) is an important transcription factor that maintains oxygen homeostasis and mediates neuroinflammation under hypoxia. However, the effect of HIF-1 on t-PA-induced HT is not clear. The aim of this study was to investigate the role of HIF-1 in t-PA-induced HT by applying YC-1, an inhibitor of HIF-1. In the present study, we found that HIF-1 expression was significantly increased in ischemic brain tissue after delayed t-PA treatment and was mainly localized in neurons and endothelial cells. Inhibition of HIF-1 by YC-1 improved infarct volume and neurological deficits. YC-1 inhibited matrix metalloproteinase protein expression, increased tight junction protein expression, and ameliorated BBB disruption and the occurrence of HT. Furthermore, YC-1 suppressed the release of inflammatory factors, neutrophil infiltration and the activation of the HMGB1/TLR4/NF-κB signaling pathway. These results demonstrated that inhibition of HIF-1 could protect BBB integrity by suppressing HMGB1/TLR4/NF-κB-mediated neutrophil infiltration, thereby reducing the risk of t-PA-induced HT. Thus, HIF-1 may be a potential therapeutic target for t-PA-induced HT.

Na+ ⁃ K+ ⁃ 2Cl- cotransporter 1 (NKCC1) which plays an important role in the dynamic balance of Cl- ions, is one of the cation⁃chloride cotransporter. It is a membrane protein that transferred the mediates Na+ , K+ and Cl- . The expression quantity or activity of NKCC1 changes with the changes in physiological and pathological conditions, thereby regulating the intracellular concentration of Cl- and the excitability of neurons. This article reviews the NKCC1's expression and regulation mode of activity as well as the effects of NKCC1 in the pathogenesis of various neurological diseases and the effects in the treatment, aiming at providing theoretical clues for the relevant future studies. doi：10.3969/j.issn.1672⁃6731.2021.03.016

目的:探讨基于优慕课+数字教材在生理学教学中的实践.方法:在2018级临床医学专业的大学生理学教学中,进行了基于优慕课+数字教材生理学理论课的研究,在学期末对学生进行问卷调查.结果:95.69％的学生认为该数字教材有助于课前的预习,96.98％的学生认为该数字教材有助于课后的复习及重点知识的掌握.98.71％的学生喜欢本章的课后小结,他们认为这可以帮助其对本章的知识点进行梳理,99.14％的学生认为可以帮助其理解知识点并喜欢同步练习,96.55％的学生认为可促进其思考问题.结论:将数字教材应用于生理学理论课的教学中,可调动学生的学习主动性,加深对所学知识的理解,帮助学生做好预习及复习,促进学生思考问题,以提高学习效果.

Mammalian oocytes within Graafian follicles are arrested at prophase I of meiosis. C-type natriuretic peptide (NPPC), secreted by mural granulosa cells (MGCs), maintains oocyte meiotic arrest via binding to its cognate receptor natriuretic peptide receptor 2 (NPR2) and producing cyclic guanosine monophosphate (cGMP). NPR2 is most concentrated in the cumulus cells. In addition, cAMP, gap junction, inosine monophosphate dehydrogenase (IMPDH) and other important regulatory factors are also involved in meiotic arrest. Luteinizing hormone (LH) then rapidly decreases cGMP and induces oocyte meiotic resumption. In this paper, advances in the molecular mechanisms of meiotic arrest and LH-induced meiotic resumption were reviewed. This paper may provide new ideas for the prevention, diagnosis and treatment of related reproductive diseases.

缺血性脑血管病（ICVD）具有高患病率、高发病率、高致残率和高死亡率的特点,其病因繁多,病理机制复杂,且脑缺血与再灌注会引起一系列细胞、分子及调节过程的变化,导致脑功能损伤。DNA甲基化是一种重要的表观遗传调控机制,多发生在基因启动子区CpG岛上,在DNA甲基转移酶的作用下建立和维持其他表观遗传学现象。DNA甲基化在ICVD的发生发展及后续治疗中发挥着作用。本文介绍了DNA甲基化在缺血性脑损伤中发挥作用的机制,对DNA甲基化成为ICVD治疗靶点的潜力进行了展望。

目的 研究匹诺塞林(pinocembrin)对高血糖诱导的大鼠卒中后出血转化的作用.方法 实验分为假手术组、大脑中动脉堵塞(MCAO)模型组、高糖+MCAO模型组、高糖+匹诺塞林+MCAO组.MCAO模型采用线栓法造模,缺血1.5 h;高糖+MCAO模型组于造模前30 min腹腔注射50％葡萄糖;高糖+匹诺塞林+MCAO组于再灌前5 min尾静脉注射匹诺塞林10 mg·kg-1.葡萄糖注射前、后30 min及MCAO术后1,2和3 h用血糖仪检测血糖.缺血24 h后,采用改良的大鼠神经功能缺损评分法进行神经学评分,TTC染色测定脑梗死体积,血红蛋白检测试剂盒检测脑组织中血红蛋白含量,伊文斯蓝渗漏实验观察对血脑屏障的影响,通过脑病理切片观察脑组织出血情况.全部实验结束后统计脑组织出血发生率和大鼠死亡率.结果 MCAO模型组各时间点血糖水平与假手术组比较均无明显变化;高糖+MCAO模型组,提前30 min腹腔注射50％葡萄糖能使血糖水平从注射前4.0升至20.9 mmol·L-1,且各时间点血糖水平均显著高于MCAO模型组(P<0.01);匹诺塞林对高糖+MCAO模型大鼠血糖水平无影响.MCAO模型组和高糖+MCAO模型组的神经学评分(分别为9.4±1.5和10.0±0.6)无显著性差异;匹诺塞林使高糖+MCAO模型大鼠神经学评分降至7.4±1.1(P<0.01).MCAO模型组脑梗体积为(23.3±11.3)％,高糖+MCAO模型组脑梗体积增加至(36.9±8.2)％(P<0.05),匹诺塞林使脑梗体积降至(26.9±5.8)％(P<0.05).与MCAO模型组相比,高糖+MCAO模型组大鼠脑组织中血红蛋白含量和伊文斯蓝含量分别由(195.5±30.1)mg·L-1和(74.6±46.8)μg·g-1组织增加至(472.0±166.9)mg·L-1(P<0.01)和(132.9±49.6)μg·g-1组织(P<0.05);匹诺塞林可显著减轻高糖+MCAO模型大鼠出血损伤,使血红蛋白含量和伊文斯蓝含量降至(299.8±47.7)mg·L-1(P<0.01)和(70.4±39.2)μg·g-1组织(P<0.05).MCAO模型组脑出血发生率和死亡率分别为18.2％和16.7％,高糖+MCAO模型组显著增加,分别为95.4％和57.3％;给予匹诺塞林后分别降至59.1％和18.9％.结论 匹诺塞林能减轻高血糖诱导的出血转化,降低出血的发生率和死亡率,是一种具有潜力的抗出血转化药物.