BACKGROUND:Post-stroke hand spasticity is a major contributor to persistent upper-limb disability and may limit the effectiveness of conventional physiotherapy. Acupuncture has been proposed as a neuromodulatory adjunct to enhance motor recovery and pain control; however, evidence from routine clinical practice remains limited. This retrospective case series investigated whether adding acupuncture to physiotherapy-based stretching results in superior functional outcomes compared with physiotherapy alone in patients with post-stroke spastic hand syndrome. METHODS:Clinical records of 13 adult stroke patients treated between 2022 and 2023 were retrospectively analyzed. Six patients received combined acupuncture and physiotherapy stretching (Group A), while seven received physiotherapy stretching alone (Group B). Acupuncture was administered twice weekly for eight weeks at Shixuan (EX-UE11), SI3, and SI4, followed immediately by standardized passive hand stretching. Outcomes were assessed using the Fugl-Meyer Assessment for the Upper Extremity (FMA-UE), including total score and subdomains (motor function, joint pain, passive joint motion, and sensation). Longitudinal changes were analyzed using linear mixed-effects models, with within- and between-group comparisons of change scores. RESULTS:From baseline to week eight, the intervention group demonstrated a significantly greater improvement in the FMA-UE motor function subscale compared with the control group (14.3 ± 4.8 vs. 7.6 ± 6.3; p < 0.05). Significant between-group differences were also observed for the hand subscale (2.7 ± 1.0 vs. 0.9 ± 1.2; p < 0.05) and the joint pain subscale (5.0 ± 4.1 vs. 0.1 ± 5.3; p < 0.05). The total FMA-UE score increased significantly more in the intervention group than in the control group over the eight-week intervention period (25.5 ± 12.3 vs. 14.3 ± 8.0; p < 0.05). No statistically significant (ns) between-group differences were identified for the upper extremity, wrist, coordination/speed, passive joint motion, or sensation subscales (p > 0.05). Within-group analyses revealed significant improvements from baseline to week eight in the intervention group for motor function, hand, joint pain, and total FMA-UE (all p < 0.05), whereas changes observed in the control group were smaller and less consistent across subscales. CONCLUSION:In this retrospective clinical analysis, acupuncture administered prior to physiotherapy stretching was associated with greater improvements in overall upper-limb motor recovery and joint pain reduction compared with physiotherapy alone in patients with post-stroke hand spasticity. These findings suggest that acupuncture may enhance conventional rehabilitation by reducing pain and facilitating motor relearning. Given the small sample size and non-randomized design, results should be interpreted cautiously. Prospective, adequately powered controlled trials are warranted to confirm efficacy and define optimal treatment protocols.

BACKGROUND:Gastrointestinal symptoms in Parkinson's disease (PD), in particular chronic constipation, are common and are treated in China using the traditional Chinese medicine (Jia-Wei-Ji-Chuan-Jian decoction) (JWJCJ)). However, information on therapeutic targets and the underlying mechanism is limited. MATERIALS AND METHODS:A total of 72 PD patients with constipation attending Departments of Neurology in Shanghai, China (Shanghai Pudong New Area Gongli Hospital and Shuguang Hospital Affiliated to Shanghai University) were recruited into the study and allocated to a Treatment group (n = 36) and a Control group (n = 36). Patients in the Control group received a combination treatment comprising anti-Parkinson agents (Western drug regimen) with the addition of a traditional Chinese patent medicine (Huang-Xing Run-Chang Tablets*) over a period of 5 weeks, whereas patients in the Treatment group received the same anti-PD Western drug regimen together with the JWJCJ decoction, also for a period of 5 weeks. An evaluation using clinical efficacy scores was carried out together with network pharmacology analysis. Identified drug targets for JWJCJ using the traditional Chinese medicine Swiss Target Prediction database (TCMSP) and disease targets for chronic constipation in PD were obtained from Genecards and the OMIM database. Therapeutic targets for JWJCJ in the treatment of chronic constipation were identified by intersecting drug targets and disease targets. GO functional enrichment analysis, KEGG pathway analysis, and disease association analysis were carried out using the DAVID database and visualized using Cytoscape 3.9.1 software. RESULTS:CSS efficacy scores in the Treatment group were higher than that in the Control group (88.57 vs. 52.94%, p < 0.001). No significant differences were seen prior to treatment in the CSS, PDQ-39 and MDS-UPDRS scores and the corresponding total scores for the two groups. After treatment, CSS values for patients in the Treatment group were higher than values before treatment (p < 0.01). Network pharmacology analysis identified 172 active components, 9,542 drug targets, and 421 intersecting target genes for JWJCJ. PPI analysis identified 10 main and possibly key targets for JWJCJ in the treatment of chronic constipation. KEGG analysis identified 198 signaling pathways, where pathways in cancer, specific cancer pathways such as prostate cancer and non-small cell lung cancer, lipid and atherosclerosis, hepatitis B, and the AGE-RAGE signaling pathway in diabetic complications were among the pathways most significantly enriched. These findings are evidence that the active ingredients in JWJCJ in the treatment of chronic constipation in PD mainly target TP53, SRC, AKT1, PIK3R1, and PIK3CA. CONCLUSION:The efficacy of JWJCJ in treating chronic constipation in PD involves the targets SRC, PIK3R1, JUN, TP53, STAT3, PIK3CA, EGFR, ESR1, MAPK1, and AKT1 domains. These findings provide theoretical basis for the clinical application of JWJCJ decoction in the treatment of chronic constipation in PD.

IMPORTANCE:Per preliminary studies, Shengdi Dahuang Decoction (SDD) is potentially effective for acute intracerebral haemorrhage (ICH); however, its effectiveness has not been rigorously assessed in extensive randomised clinical trials. OBJECTIVE:To evaluate whether SDD can improve 90-day functional outcomes in patients with ICH. DESIGN:Randomised, double-blind, placebo-controlled clinical trial included patients with acute ICH within 4 hours of symptom onset at five hospitals in Shanghai, China. INTERVENTIONS:Patients were randomised 1:1 to receive either SDD granules (each sachet contained 15 g of raw Rehmannia glutinosa and 5 g of raw rhubarb) or placebo granules orally or via a nasogastric tube (as soon as possible within 12 hours of onset, two times daily for 7 days), in addition to ICH guideline-directed treatments. Per our preclinical study, SDD reduces inflammatory injury after ICH in rats. MAIN OUTCOMES:The primary outcome measure was the proportion of patients with a score ranging 0-1 on the modified Rankin Scale (mRS) on the 90th day. RESULTS:Of the total 1211 participants with cerebral haemorrhage assessed for eligibility, 483 were enrolled. Of this, 242 participants were randomly assigned to receive SDD granules and 241 to receive placebo granules (mean age, 62.7 years; 72.9% male). Among these, 112 (46.3%) and 84 (34.9%) patients in the SDD and placebo groups, respectively, had an mRS score of 0-1 on the 90th day (adjusted relative risk 1.20, 95% CI 1.00 to 1.43; p=0.046) . The proportion of patients with poor clinical outcomes (mRS score of 5 or 6 at 90 days) was higher in the placebo group (11.2%) than in the SDD group (5.4%) (p=0.021). The 90-day mortality rate (p=0.299), 7-day National Institute of Health Stroke Scale score (p=0.583), 7-day Glasgow Coma Scale score (p=0.577), 24-hour haematoma enlargement rate (p=0.675) or 7-day relative perihaematomal oedema did not significantly differ (p=0.343) between the groups. The incidence of adverse events between the two groups did not differ significantly (p>0.05). CONCLUSIONS:In patients with acute ICH, incorporating SDD as a supplementary intervention alongside guideline-directed treatments may help enhance 90-day functional outcomes; however, more clinical trials are required to further prove its efficacy. TRIAL REGISTRATION NUMBER:NCT04200781.

Alzheimer's disease (AD) is a neurodegenerative disease with major symptoms including memory and learning deficits. Neuroinflammation associated with reactive microglia promotes AD progression. These reactive microglia secrete prostaglandins, which are synthesized through the enzymatic activity of cyclooxygenase (COX)-1 and COX-2. Here, we aimed to elucidate the specific mechanisms of COX1 in AD pathogenesis and its interactions with neuroinflammatory processes. We conducted backcrossing between COX-1 knockout (KO) and 5 × FAD mice to evaluate the effect of COX-1 deficiency on neuroinflammation. In addition, single-cell sequencing and microarray datasets from public databases and ingenuity pathway analysis in vitro were employed to explore gene expression profiles in the brains of AD mice. We identified a significant upregulation of COX-1 in 5 × FAD mice, with expression specifically localized to microglia in an age-dependent manner. Additionally, COX-1 KO alleviated neuroinflammation and accumulation of Aβ plaques, subsequently improving cognitive behavior in 5 × FAD mice. Moreover, microglia exhibited an amoeboid morphology in 5 × FAD mice, whereas in age-matched 5 × FAD/COX-1 KO mice, microglia had a ramified appearance. Additionally, our study demonstrated a pharmacological approach that inhibits the prostaglandin E2 (PGE2)/EP2 receptors via inhibition of the cAMP-PKA-NFκB-p65 pathway and NLRP3 inflammasome activation, producing similar beneficial effects as observed in COX-1 KO mice. Our findings indicate that targeting the COX-1/PGE2/EP2 signaling pathway may alleviate neuroinflammation and impede AD progression. Moreover, the EP2 receptor presents a promising pharmacological target for mitigating the pathological effects associated with COX-1 activity in AD patients.

Parkinson disease (PD) is a chronic neurodegenerative disease, and the pathgenesis is mainly related to neuronal degeneration and abnormal accumulation of αSyn. Some studies have shown that patients with PD are more likely to suffer from type 2 diabetes mellitus. Hypoglycemic drugs regulate blood glucose through modulating glucose metabolism and improving insulin sensitivity. Some of hypoglycemic drugs also have neuroprotective or antioxidant effect, and their mechanisms of action in neurodegenerative diseases have been extensively studied in recent years. This article reviews the pathological basis and related pathogenesis of PD, exploring the effect of hypoglycemic drugs on the progression of PD.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that lacks effective treatment options for the prevention of progression. Relieving swallowing difficulties, reducing breathing difficulties, and alleviating muscle spasms are essential to improving the quality of life in patients with ALS. Many symptoms can be treated clinically with medication; however, the evidence level of related research is relatively low. Rehabilitation management can aid in improving various functional impairments and enhancing quality of life. This review introduces and describes the relevant evaluations of rehabilitation and nonpharmacological symptomatic treatment methods for functional disorders from the perspectives of motor and nonmotor symptoms. This review may promote the popularization of ALS rehabilitation management and provide an additional reference for ALS treatment.

Currently, there are no effective treatments for amyotrophic lateral sclerosis (ALS), a chronic progressive neurodegenerative disease. Although the etiology of ALS is unknown, it is thought that factors such as diet, the environment, and lifestyle habits play a role. The pathogenesis of ALS includes alterations in glutamate neurotransmission, oxidative stress, mitochondrial dysfunction. Drugs such as riluzole, edaravone, dextromethorphan/quinidine combinations, and the administration of tofersen by injection are approved treatment options for ALS although a number of other agents are being examined in clinical trials. Despite these developments, the availability of effective treatment options is limited. This review summarizes the etiology and pathogenesis of ALS and describes treatments in detail as an integrative medicine approach and including traditional Chinese medicine together with the importance of the timing for interventions, precautions necessary for noninvasive ventilator and gastrostomy surgery, and precautions for dealing with respiratory issues with the overall aim of providing state-of-the-art clinical recommendations for the care and therapy of ALS patients.

Rotenone has potential chemical toxicity in the nervous system of both insects and mammals, but its deep molecular biological mechanisms have not been clarified. Here, the epigenetic regulatory mechanism underlying the toxicity of rotenone was studied using murine brain organoids (mBOs). Transmission electron microscopy indicated that rotenone destroyed mBOs'mitochondrial structure. RRBS-Seq showed that some promoter regions from the DLK1-DIO3 imprinted microRNA clusters were hypomethylated. But, rotenone stimulated hypermethylation significantly on the promoter DNA of miR-6991-3p. MiR-6991-3p in the rotenone-treated mBOs had the greatest decreased miRNA expression compared with the control. Meanwhile, luciferase report assay indicated that miR-6991-3p induced a decrease in luciferase activity via binding to specific sites on the 3'UTR of DEDD2 gene. To overexpression of miR-6991-3p attenuated mBO proliferated inhibition and cell death, accumulation for lipid peroxidation products significantly by rotenone inducing. Subsequently, results of cell staining and molecular biology experiment revealed that overexpression for miR-6991-3p significantly weakened expression levels of death-related genes (DEDD2, caspase-8, caspase-3, and caspase-1), but significantly elevated expression levels of cell proliferation-related genes (Ki67 and BCL2) in rotenone treated mBOs group. Here, we reveal a novel epigenetic mechanism of rotenone-induced neuronal death, in which rotenone induced promoter DNA hypermethylation of miR-6991-3p in the DLK1-DIO3 imprinted cluster. This caused miR-6991-3p transcriptional activity to be downregulated, which subsequently significantly increased the expression of its target gene, DEDD2, ultimately leading to neural organoid cell death.

Objective: To examine the mitochondrial protective effects of icariin, naringenin, kaempferol, and formononetin, potentially active agents in Bu-Shen-JianPi formula (BSJP) identified using network pharmacology analysis. Materials and methods: Mitochondrial protection activity was determined using a hypoxia-reoxygenation in vitro model based on the neuroblastoma cell line SH-SY5Y and measurements of anti-ferroptotic activity. Results: Icariin, naringenin, kaempferol, and formononetin showed mitochondrial protective activity involving diverse signaling pathways. The cytoprotective effects of formononetin depended on the inhibition of ferroptosis. Hypoxia-reoxygenation stimulation induced ferroptosis in SH-SY5Y cells. Discussion: Ferroptosis is a key mechanism in nervous system diseases and is associated with hypoxia-reoxygenation injury. Naringenin and kaempferol were devoid of anti-ferroptotic activity. Conclusion: Evidence has been obtained showing that the core components: of What - - - icariin, naringenin, kaempferol, and formononetin in BSJP formula have anti-hypoxic and mitochondrial protective activity of potential clinical importance in the treatment of amyotrophic lateral sclerosis and patients with symptoms of hypoxia.

BACKGROUND:There is evidence that Bu-Shen-Jian-Pi (BSJP), a traditional Chinese medicine, has curative effects in patients suffering from amyotrophic lateral sclerosis (ALS), a progressive and potentially fatal hypoxic condition.OBJECTIVE:To identify biogenic components in BSJP extracts having potential pharmacological efficacy in ALS.MATERIALS AND METHODS:Biogenic components in BSJP and their potential pharmacological targets and signaling pathways in ALS were identified and assessed using network pharmacology/hub node analysis.RESULTS:Network pharmacology analysis identified icariin, naringenin, kaempferol, quercetin, and formononetin as core components in BSJP with potential activity involving mitochondrial protection in patients with ALS.CONCLUSION:Network pharmacology analysis proved to be a successful screening tool for obtaining information from scientific databases on the pharmacology of biogenic components in BSJP showing potential therapeutic activity in ALS.

Objective: To characterize sleep duration and investigate its association with quality of life among Parkinson's Disease (PD) patients. Methods: In this multicenter cross-sectional study, 970 PD patients were divided into five groups based on selfreported sleep duration: <5,>= 5 to <6, >= 6 to <7, >= 7 to <= 8, and >8 h. The quality of life was evaluated using the 39-Item Parkinson's Disease Questionnaire (PDQ-39). Multivariable linear regression analysis, subgroup analysis, and mediation analysis were conducted to examine the association between sleep duration and quality of life. Results: In multivariable linear regression model, patients with sleep duration (<5 h) had significantly higher PDQ-39 scores (beta = 8.132, 95 % CI: 3.99 to 12.266), especially in mobility, activities of daily living, emotional well-being, stigma, social support, cognition, communication, and bodily discomfort (p < 0.05). The association between sleep duration (<5 h) and worse quality of life was more pronounced in patients with higher HY stage, longer disease duration, and sleep disorders. Moreover, a significant indirect effect of sleep duration (<5 h) on quality of life was observed, with UPDRS I, UPDRS II, and UPDRS IV scores acting as mediators. Conclusions: Short sleep duration (<5 h) is associated with worse quality of life among PD patients. This association was stronger among patients with advanced PD and sleep disorders, while non-motor symptoms and motor complications were identified as significant mediators in this association. These findings highlight the significance of adequate sleep duration and suitable interventions for sleep may help improve quality of life.

目的:探讨九雀方联合盐酸多奈哌齐片对阿尔茨海默病(AD)病人的作用及其机制.方法:选取上海市第六人民医院2019年9月—2021年9月收治的AD病人150例为研究对象.采用随机数字表法将病人分为对照组与观察组.两组均给予基础治疗,除基础治疗外,对照组给予盐酸多奈哌齐片治疗,观察组给予九雀方联合盐酸多奈哌齐片治疗.两组疗程均为3个月.治疗前后,采用蒙特利尔认知评估量表(MoCA)、简易智能精神状态检查量表(MMSE)、日常生活能力量表(ADL)、阿尔茨海默病认知功能评定量表(ADAS-cog)、阿尔茨海默病病理行为评定量表(BEHAVE-AD)、简明精神病评定量表(BPRS)评定病人认知能力、日常生活能力及精神状况,测定病人脑血管的搏动指数(PI)、平均血流速度(MFV),检测血清谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、同型半胱氨酸(Hcy)、可溶性Fas(sFas)、可溶性Fas配体(sFasL)水平.结果:与治疗前比较,治疗后两组MoCA、MMSE评分均升高,ADL、ADAS-cog、BEHAVE-AD、BPRS评分均降低(P<0.05).与对照组比较,治疗后观察组MoCA、MMSE评分均升高,ADL、ADAS-cog、BEHAVE-AD、BPRS评分均降低(P<0.05).与治疗前比较,治疗后观察组病人脑血管左侧大脑中动脉(LMCA)、左侧颈内动脉(LICA)、左侧大脑前动脉(LACA)、右侧大脑中动脉(RMCA)、右侧颈内动脉(RICA)、右侧大脑前动脉(RACA)、左侧大脑后动脉(LPCA)、左侧椎动脉(LVA)、右侧大脑后动脉(RPCA)、右侧椎动脉(RVA)及基底动脉(BA)的PI均降低,MFV均增快,差异均有统计学意义(P<0.05).与对照组比较,治疗后观察组病人脑血管LMCA、LICA、LACA、RICA、RACA、LPCA、LVA、RPCA、RVA及BA的PI均降低,MFV均增快,差异均有统计学意义(P<0.05).与治疗前比较,治疗后观察组GSH-Px、SOD、Hcy及sFas、sFasL水平均降低(P<0.01);与对照组比较,治疗后观察组GSH-Px、SOD、Hcy及sFas、sFasL均降低(P<0.01).结论:九雀方联合盐酸多奈哌齐片可以改善AD病人的认知功能、日常生活能力、精神状况及脑血管血流速度,其作用优于单用盐酸多奈哌齐片.其机制可能与降低AD病人血清GSH-Px、SOD、Hcy、sFas、sFasL水平有关.

目的:探究梓醇-川芎嗪方干预 APPswe/PS1dE9双转基因阿尔茨海默病模型小鼠的作用机制.方法:将 3 月龄 C57BL/6J野生型小鼠为对照组(control组),构建阿尔茨海默病模型后,将同月龄 APPswe/PS1dE9双转基因小鼠随机分为模型组(model组)、梓醇-川芎嗪方低剂量组(CT-L组)、梓醇-川芎嗪方中剂量组(CT-M组)、梓醇-川芎嗪方高剂量(CT-H组)、安理申组,对照组及模型组均给予生理盐水灌胃,各用药组以相应药物灌胃,每日灌胃 1次,连续 8周.对各组小鼠进行行为学观察,检测各组小鼠海马组织乙酰胆碱酯酶(AChE)、诱导型一氧化氮合酶(iNOS)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)及血清中β淀粉样蛋白 42(Aβ42).结果:行为学观察:与 model组比较,CT-M组、CT-H组、Arceipt组长时程学习和参考记忆能力、自主探究能力、情景识别记忆能力、短期工作记忆能力、条件恐惧记忆能力,缓解焦虑、抑郁状态等 7项行为学指标均明显好转(P＜0.01);与 CT-L组比较,CT-M组、CT-H组、Arceipt组 7项行为学指标均明显好转(P＜0.05或P＜0.01);与 CT-M组比较,CT-H组 7项行为学指标均明显好转(P＜0.05);与Arceipt组比较,CT-H组 7项行为学指标均明显好转(P＜0.05).生化检测方面:与 model 组比较,CT-M 组、CT-H 组、Arceipt 组海马组织 SOD、GSH-Px 水平均升高,AChE 活性、iNOS、IL-6、TNF-α、MDA水平及血清 Aβ42水平均降低,差异均有统计学意义(P＜0.01);与 CT-L组比较,CT-M组、CT-H组、Arceipt组海马组织 SOD、GSH-Px水平均升高,AChE活性、iNOS、IL-6、TNF-α、MDA水平及血清 Aβ42水平均降低,差异均有统计学意义(P＜0.05或P＜0.01);与 CT-M组比较,CT-H组海马组织 SOD、GSH-Px水平均升高(P＜0.05),AChE活性、iNOS、IL-6、TNF-α、MDA水平及血清 Aβ42水平均降低(P＜0.05);与 Arceipt 组比较,CT-H 组海马组织 SOD、GSH-Px 水平均升高(P＜0.05),AChE 活性、iNOS、IL-6、TNF-α、MDA水平及血清 Aβ42水平均降低(P＜0.05).结论:梓醇-川芎嗪方可以改善阿尔茨海默病模型小鼠的长时程学习和参考记忆能力、自主探究能力、情景识别记忆能力、短期工作记忆能力、条件恐惧记忆能力,缓解焦虑、抑郁状态,且其效应呈剂量依赖性,高剂量梓醇-川芎嗪方优于安理申.其作用机制可能与提高海马组织 SOD、GSH-Px水平,降低AChE活性及iNOS、IL-6、TNF-α、MDA、Aβ42水平有关.

帕金森病(PD)与肌萎缩侧索硬化(ALS)患者以及相关动物实验模型中,都存在血脑屏障和肠道组织屏障的破坏.近年来大量临床与基础研究证据表明,肠道和脑血管内的组织屏障破坏使得中枢神经系统更易受外部因素的影响,成为PD和ALS潜在发病机制之一.肠道屏障、血脑屏障等研究对于诊治PD、ALS、提供了新的治疗靶点.除此之外,中医以脾胃为作用靶点,以调节脾胃功能治疗类似PD、ALS症状的患者也显示出一定疗效.因此,中西医结合通过修复组织屏障有可能成为未来神经退行性疾病的一个新的治疗靶点.文中综述了组织屏障功能与PD和ALS的发病以及进展的关联性研究,探讨中西医结合治疗的新型干预策略在PD、ALS患者组织屏障治疗中的应用.

目的:探讨九雀方联合盐酸多奈哌齐片对血瘀证阿尔茨海默病(AD)病人舌下络脉及其血清血小板活化因子(PAF)、血管内皮生长因子(VEGF)水平的影响.方法:选取2019年5月—2021年5月于上海市第六人民医院就诊的AD血瘀证病人120例,按照随机数字表法分为对照组和干预组,每组60例.两组均给予基础治疗,同时对照组给予盐酸多奈哌齐片治疗,干预组给予九雀方联合盐酸多奈哌齐片治疗.两组疗程均为3个月.观察比较治疗前后两组病人疾病认知、舌下络脉变化及其血清PAF、VEGF的表达水平.结果:与治疗前比较,治疗后两组阿尔茨海默病评定量表认知部分(ADAS-cog)评分、日常生活功能量表(ADL)评分、神经精神科问卷(NPI)评分及舌下络脉积分均下降,蒙特利尔认知评估量表(MoCA)评分和简易智能量表(MMSE)评分、血清PAF及VEGF水平均升高,差异均有统计学意义(P<0.05或P<0.01).治疗后,与对照组比较,干预组ADAS-cog评分、ADL评分、NPI评分及舌下络脉积分下降更明显,MoCA评分和MMSE评分、血清PAF及VEGF水平升高更明显,差异均有统计学意义(P<0.05).对照组不良反应发生率为3.45％,干预组不良反应发生率为5.08％,两组比较差异无统计学意义(P>0.05).结论:九雀方联合盐酸多奈哌齐片可以改善血瘀证AD病人的认知功能,其可能通过降低AD病人舌下络脉积分、提高血清PAF及VEGF水平从而发挥治疗血瘀证AD的作用.

EDITORIAL article Front. Neurol., 16 January 2023Sec. Neuromuscular Disorders and Peripheral Neuropathies Volume 13 - 2022 | https://doi.org/10.3389/fneur.2022.1105360

目的 探讨恒清Ⅳ号方对帕金森病(PD)大鼠模型睡眠障碍的作用及其机制.方法 选取60只Wistar大鼠,采用6-羟基多巴(6-OHDA)建立PD大鼠模型.造模4周后,腹腔注射阿扑吗啡(apomorphine)诱发旋转实验进行PD模型鉴定,造模成功的大鼠随机分为模型组、恒清Ⅳ号方低剂量(LD)组、恒清Ⅳ号方中剂量(MD)组及恒清Ⅳ号方高剂量(HD)组,每组10只;另选取10只正常大鼠作为正常组.LD组、MD组和HD组大鼠分别给予相应剂量的恒清Ⅳ号方溶液,正常组和模型组大鼠灌胃等量生理盐水.采用脑电图(EEG)和肌电图(EMG)记录各组大鼠睡眠时间,高效液相色谱法(HPLC)检测各组大鼠纹状体中多巴胺(DA)及5-羟色胺(5-HT)含量.结果 与模型组比较,LD组、MD组和HD组大鼠总睡眠时间(TST)延长,觉醒时间(AT)缩短,慢波睡眠时间(SWST)、快波睡眠时间(FWST)延长(P<0.05);与LD组比较,MD组、HD组大鼠TST延长,AT缩短,SWST、FWST延长(P<0.05);与MD组比较,HD组大鼠TST延长,AT缩短,SWST、FWST延长(P<0.05).疗效与剂量呈正相关.与模型组比较,LD组、MD组和HD组大鼠纹状体DA、5-HT水平升高(P<0.05);与LD组比较,MD组、HD组大鼠纹状体DA、5-HT水平升高(P<0.05);与MD组比较,HD组大鼠纹状体DA、5-HT水平升高(P<0.05).PD大鼠模型的纹状体DA、5-HT水平均与恒清Ⅳ号方剂量呈正相关.结论 恒清Ⅳ号方可以改善PD大鼠模型的睡眠障碍,且量效关系呈正相关,其可能通过提高纹状体中DA、5-HT含量而发挥作用.

目的 观察恒清Ⅲ号方治疗缺血性脑卒中(IS)合并脑叶微出血(CMBs)的临床疗效,并分析其作用机制.方法 选取2019年11月—2020年10月上海交通大学附属第六人民医院收治的缺血性脑卒中合并脑叶微出血病人125例为研究对象,采用随机数字表法分为治疗组(63例)与对照组(62例).对照组给予基础治疗,治疗组在基础治疗上加用恒清Ⅲ号方.两组疗程均为8周.比较两组临床疗效、美国国立卫生研究院脑卒中量表(NIHSS)评分、改良Rankin量表(mRS)评分、脑叶微出血病灶数目及血清白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、钙结合蛋白100B(S100B)、血管内皮生长因子(VEGF)水平.结果 治疗组总有效率为87.30％,高于对照组的61.29％(P<0.01).治疗后,治疗组NIHSS评分、mRS评分低于对照组,脑叶微出血病灶数目少于对照组,差异均有统计学意义(P<0.05或P<0.01);治疗组治疗后血清IL-1、IL-6、TNF-α、S100B水平低于对照组(P<0.01),VEGF水平高于对照组(P<0.01).治疗过程中治疗组未发现明显不良反应.结论 恒清Ⅲ号方可能通过减轻炎症反应、促进血管形成、改善神经功能,从而治疗缺血性脑卒中合并脑叶微出血.

Introduction Positive effects have been observed when the traditional Chinese medicine Hua Tuo Zai Zao Wan (HTZZW) has been used for the treatment of atherosclerosis (AS), although with an unclear mechanism. Methods ApoE-/- C57/BALB mice were used to determine the efficacy of HTZZW by blood lipid biochemical analysis and histopathology H&E staining. qPCR and western blot were used to determine the expression of METTL3/14 and NF-κB. Results High-fat diet-fed ApoE-/- mice that consumed HTZZW exhibited significantly smaller plaque areas and significantly decreased unstable collagen areas in the aortic arch as well as significantly lower blood levels of total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol compared with the control group. Consumption of HTZZW significantly decreased the proportion of Mφ1 in the peripheral blood. HTZZW not only inhibited the expression of m6A methyltransferases METTL14, METTL3, and overall RNA methylation level, but it also decreased the m6A modification level on specific sites of NF-κB mRNA. Conclusion HTZZW significantly alleviated the progression of AS by regulating the expression of the m6A methyltransferases METTL14 and METTL3 in macrophages, eliminating m6A modifications of NF-κB mRNA, influencing the stability of NF-κB mRNA, and ultimately resulting in the deactivation of inflammatory macrophages.