Formononetin has been demonstrated to protect against cerebral ischemia-reperfusion injury, however its mechanism has to be further researched. This study examined the effect of formononetin on cerebral ischemia-reperfusion injury in rats using the PARP-1/PARG/Iduna signaling pathway. In male SD rats, a model of cerebral ischemia-reperfusion injury was developed. Animals were randomly assigned to one of eight groups: Sham operation, Sham operation + formononetin, MCAO, MCAO + formononetin, PARP inhibitor (PJ34) + MCAO, formononetin + PJ34 + MCAO, PARG inhibitor (Ethacridine lactate) + MCAO, and ethacridine lactate + formononetin. The neurological deficit test, TTC staining, HE staining, Nissl staining, TUNEL staining, and western blotting were utilized to assess formononetin's protective effects in MCAO rats. The data show that formononetin can effectively alleviate neurological dysfunction and pathological changes in brain tissue in rats with cerebral ischemia-reperfusion injury, reduce the area of cerebral infarction and neuronal apoptosis, decrease the protein levels of PARP-1, PARG, Caspase-3, P53, and AIF in brain tissue, and increase the protein levels of Iduna and p-AKT. As a result, we concluded that formononetin improves brain ischemia-reperfusion injury in rats by modulating the PARP-1/PARG/Iduna signaling pathway.

Spinal cord stimulation (SCS) has emerged as a potential therapeutic tool for various chronic conditions, but its efficacy in post-operative wound healing for multiple sclerosis (MS) patients has not been comprehensively understood. This meta-analysis aimed to evaluate the impact of SCS on post-operative wound healing and scar formation in MS patients. A systematic literature review identified seven studies for inclusion. We focused on wound healing as measured by the redness, edema, ecchymosis, discharge, approximation (REEDA) scale 1 week post-operation and scar formation assessed by the Manchester Scar Scale (MSS) 3 months post-operation. The results demonstrated a significant improvement in wound healing in the SCS group, with a standard mean difference (SMD) of -5.82 (95% confidence interval [CI]: [-7.56, -4.09], p < 0.01) on the REEDA scale. For scar formation, the SCS group showed a notable reduction in MSS scores, with an SMD of -10.06 (95% CI: [-14.53, -5.58], p < 0.01). These findings underscore the potential of SCS as an adjunct therapy in enhancing surgical recovery in MS patients, pointing towards its broader applications in post-operative care.

Objective To report the clinical manifestation and genetic characteristics of a patient having frontotemporal dementia (FTD) with abnormal behavior and unstable walking. Methods The clinical and imaging features of a patient who was eventually diagnosed with FTD were analyzed. The patient’s neuropsychological, PET-CT, electromyography, and genetic data were collected. Furthermore, the patient’s blood samples were examined for FTD-related genes. Results The patient was a 52-year-old man with hidden onset. The symptoms progressed gradually, presenting with abnormal behaviors, including repeated shopping, taking away other people’s things, constantly eating snacks, and frequently calling friends at night. The patient also exhibited executive dysfunction, such as the inability to cook and multiple driving problems, e.g., constantly deviates from his lane while driving. In addition, the patient showed personality changes such as irritability, indifference, and withdrawal, as well as motor symptoms, including unstable walking and frequent falls when walking. Brain magnetic resonance imaging revealed hippocampal sclerosis along with widening and deepening of the bilateral temporal lobe sulcus. Brain metabolic imaging via PET-CT demonstrated decreased metabolism in the bilateral prefrontal lobe, with the abnormal energy metabolism indicating FTD. Lastly, blood sample analysis detected mutations in the amyotrophic lateral sclerosis (ALS)-related GRN gene c.1352C > T (p.P451L) and ErbB4 gene c.256 T > C (p.Y86H). Conclusion This is the first case of heterozygous mutations in the GRN and ErbB4 genes in FTD alone. The GRN and ErbB4 genes are likely to be important in the pathogenesis of FTD, expanding the common genetic profile of ALS and FTD.

Background Atherosclerosis(AS) poses a pressing challenge in contemporary medicine. Formononetin (FMN) plays a crucial role in its prevention and treatment. However, the detailed impact of FMN on the stability of atherosclerotic plaques and its underlying mechanisms remain to be elucidated. Methods An intervention consisting of FMN was given along with a high-fat food regimen in the ApoE-/- mouse model. The investigation included the evaluation of the degree of atherosclerotic lesion, the main components of the plaque, lipid profiles, particular markers indicating M1/M2 macrophage phenotypes, the quantities of factors related to inflammation, the infiltration of macrophages, and the identification of markers linked to the α7nAChR/JAK2/STAT3 axis effect molecules. Results The evaluation of aortic morphology in ApoE-/-mice revealed that FMN significantly improved the plaque area, fibrous cap protrusion, lipid deposition, and structural alterations on the aortic surface, among other markers of atherosclerosis,and there is concentration dependence. Furthermore, the lipid content of mouse serum was assessed, and the results showed that the low-, medium-, and high-dosage FMN groups had significantly lower levels of LDL-C, ox-LDL, TC, and TG. The results of immunohistochemical staining indicated that the low-, medium-, and high-dose FMN therapy groups had enhanced CD206 expression and decreased expression of CD68 and iNOS. According to RT-qPCR data, FMN intervention has the potential to suppress the expression of iNOS, COX-2, miR-155-5p, IL-6, and IL-1β mRNA, while promoting the expression of IL-10, SHIP1, and Arg-1 mRNA levels. However, the degree of inhibition varied among dosage groups. Western blot investigation of JAK/STAT signaling pathway proteins and cholinergic α7nAChR protein showed that p-JAK2 and p-STAT3 protein expression was suppressed at all dosages, whereas α7nAChR protein expression was enhanced. Conclusions According to the aforementioned findings, FMN can reduce inflammation and atherosclerosis by influencing macrophage polarization, blocking the JAK/STAT signaling pathway, and increasing α7nAChR expression.

Ischemic stroke, caused by diminished or interrupted cerebral blood flow, triggers the activation of microglial cells and subsequent inflammatory responses. Formononetin (FMN) has been observed to inhibit BV2 microglial cell activation and alleviate ensuing neuroinflammatory reactions. Despite extensive research, the precise underlying mechanism remains unclear. To investigate the neuroinflammatory response following FMN-mediated inhibition of BV2 microglial activation, we employed an in vitro oxygen-glucose deprivation/reperfusion (OGD/ R) model. BV2 microglial cells were categorized into four groups: control, FMN, OGD/R, and OGD/R+FMN. Cell viability was assessed using the CCK-8 assay, while flow cytometry assessed M1 and M2 cell populations within BV2 cells. Immunofluorescence was utilized to detect the expression levels of apoptosis-inducing factor (AIF), p53, Toll-like receptor 4 (TLR4), and NF-kappa B p65. Western blotting (WB) was conducted to quantify p65/p-p65, I kappa B-alpha/p-I kappa B-alpha, and TLR4 protein levels in each group. Additionally, ELISA was employed to measure IL-1(3 and TNF-alpha levels in cell supernatants from each group. The results revealed a significant increase in the proportion of iNOS/CD206-positive M1/M2 cells in the OGD/R group compared to the control group (p < 0.05). There was also a notable increase in nuclear translocation of NF-kappa B p65 and elevated expression of inflammatory factors IL1(3 and TNF-alpha in cell supernatants. Moreover, levels of p-p65, p-I kappa B-alpha, and TLR4 proteins were significantly elevated in the OGD/R group (p < 0.05). However, the addition of FMN reversed these effects. Specifically, FMN administration notably attenuated cell death and inflammation in BV2 microglia induced by OGD/R through modulation of the TLR4/NF-kappa B signaling pathway.These findings suggest that FMN may serve as a potential therapeutic agent against neuroinflammation associated with ischemic stroke by targeting microglial activation pathways.

[目的]运用数据挖掘技术探讨中医药治疗后循环缺血性眩晕的用药规律.[方法]检索2004—2019年治疗后循环缺血性眩晕的相关文献,根据纳入标准和排除标准选择符合要求的文献,将处方内容记录到数据库中,通过SPSS 25.0和IBM SPSS Modeler 18软件分析用药频率、频数及关联性,揭示治疗后循环缺血性眩晕的用药规律.[结果]筛选出相关文献186篇,纳入治疗后循环缺血性眩晕处方210首,涉及中药种类173味,使用频数2302次,其中天麻、川芎和半夏的使用频率最高.药物类别以补虚药、活血化瘀药、息风止痉药、平肝潜阳药、解表药、利湿药为主.证型分布前3位依次为气血亏虚型、瘀血阻窍型、风痰上扰型.采用Apriori算法进行关联分析,支持度≥10％时支持度前10位的药对基本以补虚药、平肝潜阳药、息风止痉药、活血化瘀药及解表药为主.[结论]中医药治疗后循环缺血性眩晕以补虚药最为多见,其次是平肝潜阳药、息风止痉药、活血化瘀药、解表药,药组与药对基本上是补虚药、平肝潜阳药、息风止痉药、行气药、利水消肿药、解表药及活血化瘀药的不同组合,证型与用药方面关系密切.虚损是根本原因,风、痰、瘀为标,应以补虚泻实为原则,权衡标本缓急.

血液透析是肾衰竭最常见的治疗方式,几乎90％的患者选择血液透析,功能正常的血管通路是提供充分血液透析治疗的关键[1].维持血管通路通畅对血液透析患者来说是一个巨大的挑战,"天然"动静脉内瘘( arteriovenous fistula,AVF)目前被推荐为主要血管通路[2,3].新生内膜增生引起的内膜狭窄是血管通路功能障碍的最常见原因.传统球囊血管成形术对于内膜增生型狭窄即时效果差,远期通畅率低[4,5].

目的:运用数据挖掘技术分析针灸治疗眼肌痉挛的临床取穴特点和规律.方法:检索2000年至2019年针灸治疗眼肌痉挛的临床文献,根据纳入标准和排除标准筛选出符合要求的文献,建立眼肌痉挛的针灸临床处方数据库,使用SPSS 25.0和IBM SPSS Modeler 18.0软件进行频次、关联规则分析和聚类分析,揭示针灸治疗眼肌痉挛的用穴规律.结果:筛选出相关文献77篇,纳入针灸处方89条,涉及腧穴87个,使用频数669次.其中攒竹、合谷、四白、风池使用频率最高.所选经脉以足阳明胃经使用频数最高,其次是足少阳胆经、足太阳膀胱经、经外奇穴.聚类分析显示存在10个核心用穴群及重点穴位.关联规则显示,穴位之间相关性最高的是合谷+风池、攒竹+太阳、合谷+太冲、攒竹+丝竹空、合谷+足三里.结论:针灸治疗眼肌痉挛的选穴以辨证施治为原则,遵循近部选穴、远部选穴原则以及相应的配穴方法,既能将腧穴协同增效的作用充分发挥,又能促进运动、感觉功能恢复.

目的:基于中医通腑理论的内涵,利用数据挖掘中医药治疗缺血性中风的核心药物,并对核心药物进行有效评价,旨在阐明核心药物治疗缺血性中风中的“通腑”机制.方法:通过文献检索,收集2005年至2020年运用通腑理论诊治缺血性中风的相关文献,运用SPSS 25.0统计软件发现处方中的核心药物,并选用核心药物活性成分进行有效评价:通过建立大脑中动脉栓塞(MCAO)脑缺血大鼠模型,并将其分为假手术组(SHAM组)、模型组(MCAO组)、米诺环素组、大黄素高、中、低剂量组(1.404 mg/kg.d-1、0.702 mg/kg.d-1、0.351 mg/kg.d-1).采用Longa评分法测量神经功能缺损评分,2,3,5-氯化三苯基四氮唑(TC)染色显示计算大鼠脑梗死面积百分比,Western Blot检测各组大鼠缺血半暗带区TLR4、MMP-9的表达变化.免疫荧光染色检测大鼠缺血周边区小胶质细胞活化.结果:共检索到有关通腑法治疗缺血性中风相关文献报道235篇,应用处方明确的中药方剂232个,涉及中药208味,其中以大黄使用频率最高.动物实验结果显示,与假手术组比较,模型组大鼠神经功能评分、脑梗死面积百分比明显增高(P＜0.05).与模型组比较,各药物组大鼠神经功能评分、脑梗死面积百分比(P＜0.05或P＜0.01).与假手术比较,模型组TLR4、MMP-9蛋白表达水平显著升高,差异具有统计学意义(P＜0.05);与模型组比较,除大黄素低剂量组大鼠脑缺血周边区MMP-9蛋白表达水平降低不显著外,其余各组大鼠上述指标均明显改善(P＜0.05或P＜0.01).免疫荧光染色结果显示,脑缺血周边区可见活化状态的小胶质细胞,而药物组均可不同程度降低小胶质细胞免疫荧光表达.结论:“通腑”核心药物大黄及其活性成分可抑制脑缺血损伤后小胶质细胞诱导的炎症反应,其机制可能与TLR4/MMP-9信号通路失活有关.

目的:本研究旨在探讨大黄酸对脑缺血损伤后水通道蛋白4(AQP4)与脑水肿的影响以及小胶质细胞介导的炎症在此过程中的作用.方法:选择改良线栓法建立大鼠右侧大脑中动脉栓塞(MCAO)的脑缺血模型,并将其分为假手术组、模型组、米诺环素组和大黄酸高、中、低剂量组(346,1.73,0.865mg·kg-1).通过改良神经行为学评分测量神经行为功能.采用干湿重法测定脑缺血损伤大鼠脑组织含水量变化.蛋白免疫印迹法(Western blot)检测各组大鼠脑缺血周边区γ-干扰素(IFN-γ),白细胞介素-2(IL-2)的表达变化.免疫荧光双标记法检测小胶质细标记物离子钙接头蛋白抗原-1(Iba-1),AQP4蛋白的表达和定位.结果:与假手术组比较,模型组大鼠神经功能评分、脑组织损伤侧含水量明显增高(P＜0.05);与模型组比较,各药物组大鼠神经功能评分、脑组织含水量均明显降低(P＜0.05,P＜0.01);与假手术组比较,模型组IFN-y,IL-2蛋白表达水平明显升高(P＜0.05);与模型组比较,各药物组脑缺血周边区IFN-γ,IL-2蛋白水平均明显改善(P＜0.05,P＜0.01).与假手术组比较,模型组可见激活的小胶质细胞上AQP4蛋白荧光表达明显增强;与模型组比较,各药物组可减少激活的小胶质细胞上AQP4蛋白荧光的表达,各组大鼠脑缺血周边区可见不同程度激活的小胶质细胞标记物Iba-1与AQP4共定位表达.结论:大黄酸可以减轻脑缺血损伤引起的脑水肿程度,其机制可能与其抑制小胶质细胞介导的神经炎症、下调AQP4蛋白表达有关.

目的 观察大黄素对大鼠脑缺血损伤模型后离子型钙接头蛋白-1(Iba-1)、基质金属蛋白酶-9(MMP-9)、Toll样受体4(TLR4)、核因子kappa B(NF-κB)和细胞间黏附分子-1(ICAM-1)、肿瘤坏死因子(TNF-α)的影响,探讨大黄素对脑缺血后小胶质细胞活化的作用及其可能的保护机制.方法 将120只Sprague-Dawley大鼠随机分为假手术组、模型组、米诺环素组(阳性对照,45mg/kg)以及大黄素高、中、低剂量组(1.404,0.702,0.351mg/kg).采用线栓法建立大脑中动脉闭塞(MCAO)模型,脑缺血2h后,各给药组大鼠腹腔注射相应药物,假手术组、模型组给予等体积生理盐水,每日1次,连续治疗7d.采用Longa评分法测量神经功能缺损评分,2,3,5-氯化三苯基四氮唑(TTC)染色显示计算大鼠脑梗死面积百分比,Western Blot检测各组大鼠缺血半暗带区TLR4、NF-κB、ICAM-1和TNF-α蛋白的表达变化.免疫荧光双标记法检测小胶质细标记物Iba-1与MMP-9蛋白的表达和定位.结果 脑缺血7d后,与假手术组相比较,模型组大鼠的神经功能评分及脑梗死面积百分比均显著升高(P＜0.05).与模型组相比较,各给药组神经功能损伤评分及脑梗死面积百分比均显著降低(P＜0.05或P＜0.01),且具有一定量效关系.与假手术组比较,模型组可见大量激活的小胶质细胞上MMP-9蛋白荧光表达增强,而大黄素各剂量组明显减少小胶质细胞上MMP-9蛋白荧光表达.与假手术比较,模型组TLR4、NF-κB、ICAM-1和NF-κB蛋白表达水平显著升高,差异均有统计学意义(P＜0.05);与模型组相比较,除大黄素高剂量组大鼠脑缺血周边区ICAM-1蛋白表达水平表达降低不显著外,其余各组上述蛋白水平表达均明显改善(P＜0.05或P＜0.01).结论 大黄素可能通过抑制TLR4/NF-KB通路介导的小胶质细胞活化及其炎症因子的释放发挥脑保护作用.

目的:基于数据挖掘方法探讨中药复方治疗周围性面瘫的组方用药规律.方法:检索近30年来中国知网数据库、万方数据库、重庆维普数据库、中国生物医学库等中文数据库中治疗周围性面瘫的中药复方文献.通过Excel建立中药数据库,应用"古今医案云平台V 2.0"软件分析药物的使用频次、功效、中医证型、关联规则等,总结中药处方的用药特点.结果:筛选出符合纳入标准的中药复方文献共89篇,涉及121份处方及156味中药.药物使用频次累计1354次,使用频次排列在前10的中药分别是僵蚕、全蝎、制白附子、川芎、当归、防风、蜈蚣、黄芪、地龙、甘草,用药类别以息风止痉药、补虚药、活血化瘀药为主.中医证型主要以风痰阻络证为主,风寒袭络证、气血亏虚证等次之.中药配伍关联分析结果显示高频的药对主要是僵蚕、全蝎、制白附子之间的相互配伍.结论:中医药治疗周围性面瘫组方用药规律以祛风为主,药物之间配伍关联多以牵正散为核心组方,根据不同证型辅以清热、益气、活血等治疗.其中,僵蚕、全蝎、白附子、川芎、当归、防风等6种药物组成了治疗周围性面瘫的基本框架.

新型冠状病毒肺炎(COVID-19)已在全球许多国家蔓延,该病毒与SARS-C oV和MERS-CoV虽然有相似性,但截然不同.本文就新型冠状病毒的病原学、流行病学及预防控制等方面的研究现状进行综述,以期对新冠肺炎的防治提供借鉴.

目的 基于数据挖掘技术,探索现代中医药治疗中风病的临床用药规律及特点.方法 在中国知网搜集中医治疗中风病的文献,整理筛选后,使用SPSS 22.0分析药物的使用频次、功效分析、高频聚类分析等.结果 对筛选出的145首处方进行分析,中药高频率使用前五位排名分别是:当归、地龙、川芎、黄芪、石菖蒲,功效多以活血化瘀、平肝息风为主,高频聚类分析提示中风处方药物组成多以镇肝熄风、活血化瘀为主.结论 镇肝熄风、活血化瘀法为中医临床治疗中风病较为常见及有效的方法.

目的 观察大黄酚对脂多糖(LPS)激活诱导的小胶质细胞炎性反应的影响并探讨其作用机制.方法 采用LPS诱导小胶质细胞活化,CCK-8检测不同浓度大黄酚(1、10、50、100μg/ml)对小胶质细胞细胞活性的影响,将细胞分为空白组、LPS组、LPS+大黄酚低、中、高剂量组(1、10、50μg/ml),一氧化氮(NO)测试盒检测细胞上清液中NO释放量,ELISA检测IL-1、TNF-a、IL-4和IL-10含量,蛋白免疫印迹法检测小胶质细胞NF-κB及TLR4蛋白表达的情况,免疫荧光法检测NF-κB蛋白在细胞中的位置变化.结果 大黄酚浓度在1～50μg/ml对小胶质细胞活力影响不显著,此浓度范围内,大黄酚呈剂量依赖性地降低IL-1、TNF-a表达水平,升高IL-4、IL-10的表达水平(<0.05);此外,大黄酚可抑制LPS诱导的小胶质细胞形态改变.与空白组比较,LPS组TLR4、NF-kB蛋白表达水平升高意义(<0.05);与LPS组相比较,除LPS+大黄酚低剂量组胞核中NF-κB蛋白表达水平降低不显著外,其余各组上述蛋白水平表达均改善(<0.05).免疫荧光染色实验结果显示,与空白组相比较,LPS组细胞核中NF-κB蛋白表达上升,胞浆中NF-κB表达下降.结论 大黄酚可以抑制LPS诱导的小胶质细胞炎性反应,促进小胶质细胞M1型向M2型的转化,其机制可能与下调TLR4/NF-κB信号通路有关.

目的:研究大黄酚对脑缺血损伤模型大鼠小胶质细胞活化及炎症因子表达的影响.方法:将SD大鼠随机分为假手术组、模型组和大黄酚高、中、低剂量组[7.88、3.94、1.97 mg/(kg·d)],每组20只(复制模型过程中如死亡或造模不成功则补足).除假手术组外,其余各组大鼠均采用改良线栓法建立中动脉闭塞模型.于缺血2 h后,假手术组和模型组大鼠腹腔注射生理盐水1 mL,各给药组大鼠腹腔注射相应药液1 mL,每日1次,连续给药7 d.末次给药后,记录各组大鼠神经功能缺损评分,采用TTC染色法观察大鼠脑组织梗死情况并计算脑梗死面积百分比,采用免疫荧光染色法观察大鼠脑缺血半暗带区Iba-1阳性细胞的表达情况,采用Western blotting法检测大鼠脑缺血半暗带区Notch-1、肿瘤坏死因子α(TNF-α)、细胞间黏附分子1(ICAM-1)蛋白的表达情况.结果:假手术组大鼠脑组织未见梗死区域;其脑缺血半暗带区Iba-1阳性细胞较少且呈分枝状.与假手术组比较,模型组大鼠脑组织梗死区域明显;脑缺血半暗带区Iba-1阳性细胞明显增多,且呈阿米巴形或圆形;其神经功能缺损评分、脑梗死面积百分比以及脑缺血半暗带区Notch-1、TNF-α、ICAM-1蛋白的相对表达水平均显著升高(P<0.05).与模型组比较,大黄酚各剂量组大鼠脑组织梗死区域均有不同程度缩小;脑缺血半暗带区Iba-1阳性表达细胞有所减少;其神经功能缺损评分、脑梗死面积百分比以及脑缺血半暗带区Notch-1、TNF-α、ICAM-1蛋白的相对表达水平均显著降低(P<0.05或P<0.01).结论:大黄酚对脑缺血损伤模型大鼠具有一定的脑保护作用,可减轻其神经损伤;其机制可能与抑制Notch信号通路介导的小胶质细胞活化及炎症因子的表达有关.

目的:研究奥拉西坦治疗脑梗死急性期合并认知功能障碍的临床效果.方法:选取脑梗死急性期合并认知功能障碍患者94例,采用随机数字表法分为两组,对参照组(n=47)采用常规疗法,实验组(n=47)在参照组基础上加用奥拉西坦治疗,对比二组患者的认知功能、日常生活能力及不良反应.结果:实验组患者MMSE评估值、ADL评估值均优于参照组,组间对比P<0.05;二组患者的不良反应发生率比较无差异,P>0.05.结论:应用奥拉西坦治疗脑梗死急性期合并认知功能障碍,效果理想,对恢复认知功能、提高生活自理能力均有积极帮助,且不良反应少、安全性高,值得推广.

目的:研究干扰素在多发性硬化治疗中的应用效果及价值.方法:选取我科在2016年1月--2018年12月收治的88例多发性硬化患者,采用抽签法分为两组,参照组(n=44)予以常规治疗方案,实验组(n=44)在参照组基础上加用干扰素β-1b,对比二组患者的治疗总有效率及血清指标.结果:实验组患者的治疗总有效率为93.18％,明显高于参照组的68.18％,实验组患者的IFN-γ、IL-10、IL-6各指标均优于参照组,两组数据比较P<0.05.结论:为多性硬化患者采用β-干扰素治疗,可促进神经功能恢复、减轻机体炎性反应,是一种值得推广的治疗方案.

近年研究表明,氧化应激损伤在脑缺血再灌注损伤中起重要作用.近来,大量研究报道大黄及其活性成分对脑缺血再灌注损伤具有脑保护作用,其作用机制与抗氧化作用密切相关,但其涉及的研究较多,如大黄酚、大黄素、大黄素甲醚、芦荟大黄素、大黄酸等,具体机制尚不清楚.为此,本文从抗氧化方面总结大黄游离蒽醌类成分对脑缺血再灌注损伤的脑保护机制,以期为临床运用和进一步研究提供参考.