Metabolic dysfunction-associated steatohepatitis (MASH) is driven by complex intercellular communication and regulated cell death pathways. Mitoxyperilysis, a recently characterized form of regulated lytic cell death, remains poorly defined in MASH. Here, we integrated multiomics, cross-species transcriptomics, machine learning, and in vivo models to dissect mitoxyperilysis activation and its therapeutic relevance in MASH. Single‑cell and spatial transcriptomic datasets from mouse and human MASH livers were analyzed. Cell–cell communication was inferred using CellChat, and metabolite‑mediated cell–cell communication (mCCC) was assessed with MEBOCOST. Mitoxyperilysis activity was scored via AUCell and AddModuleScore. Eleven machine learning classifiers identified transcriptomic signatures distinguishing MASH from controls, and key regulators were subjected to in silico knockout (scTenifoldKnk). A choline‑deficient, L‑amino acid‑defined high‑fat diet (CDAHFD) mouse model was used for in vivo validation. Single‑cell profiling revealed that mitoxyperilysis activity was highly enriched in myeloid cells, particularly monocyte‑derived macrophages (Mo‑Macrophages) and neutrophils, and was strongly induced by high‑fat high‑sucrose diet. CellChat and mCCC analyses demonstrated that Mo‑Macrophages served as central hubs of rewired inflammatory and metabolic crosstalk in MASH. Spatial transcriptomics confirmed the expansion of pro‑inflammatory hepatocyte subsets and conserved upregulation of mitoxyperilysis components (e.g. BAX, TLR4, NINJ1) in both mouse and human MASH. Cross‑species profiling across mouse, rat, hamster, non‑human primate, and human datasets demonstrated evolutionarily conserved activation of the entire mitoxyperilysis pathway. Machine learning identified Bax as the sole overlapping driver gene linking diet‑induced transcriptomic signatures to mitoxyperilysis. In silico Bax ablation perturbed lipid metabolism and immune pathways. In CDAHFD-induced MASH mice with typical pathological phenotypes, core mitoxyperilysis genes were transcriptionally upregulated, and Bax/Bid/Bak1 upregulation was validated at the protein level. While RhoA mRNA increased, total RhoA protein remained stable, with its ubiquitination elevated and activity suppressed. Mitoxyperilysis is an evolutionarily conserved, myeloid‑enriched pathway activated in MASH. Bax acts as a critical regulatory node, while RhoA is modulated via ubiquitination and functional suppression. Targeting this axis may provide a novel therapeutic strategy for MASH.

This study aimed to explore the relationships between lipid metabolism indices—the Lipid Accumulation Product (LAP), Visceral Adiposity Index (VAI), Cardiac Metabolic Index (CMI), and Atherogenic Index of Plasma (AIP)—and sarcopenia in individuals aged ≥ 60 years, and to investigate the mediating role of uric acid (UA) in these relationships. The goal was to provide scientific evidence and practical guidance for preventing and treating sarcopenia in older adults. Data from 2001 participants aged ≥ 60 years in the 2003–2006 National Health and Nutrition Examination Survey (NHANES) were analyzed. Statistical analyses, including logistic regression, restricted cubic splines (RCS), subgroup analysis, and mediation analysis, were conducted to examine the associations among various lipid metabolism indices, UA levels, and sarcopenia. Multivariable-adjusted models revealed significant inverse associations between lipid metabolism indices and sarcopenia (all P < 0.05). In the fully adjusted model (model III), the adjusted odds ratios (OR) for LAP, VAI, CMI, and AIP were 0.97 (95

The treatment of pre-diabetes mellitus (pre-DM) currently includes lifestyle intervention, modern medicine treatment, and traditional Chinese medicine(TCM) synthetic therapy. TCM has shown curative effects in pre-DM treatment, including Chinese herbal compounds, Chinese patent medicine, acupuncture, massage, exercise, and other therapies. However, the existing studies seldom treat patients with pre-DM based on syndrome differentiation, and the essence of TCM is treatment based on syndrome differentiation. Therefore, a unique survey of patients with pre-DM of a particular TCM syndrome type is necessary, and this study will focus on patients with spleen deficiency and phlegm turbidity in pre-DM. A single-center, randomized, double-masked, and placebo-controlled trial is planned. A total of 186 patients will be enrolled in the study. Participants will be randomly assigned to the experimental or control group in a 1:1 ratio. The experimental group will be treated with Tangdi prescription (TDP) granule combined with healthy lifestyle intervention, and the control group will be treated with TDP placebo combined with healthy lifestyle intervention. This study will take 3 weeks as a course of treatment for 4 classes, and will be followed up at 3rd, 6th, 9th, and 12th weeks during the treatment period. The primary outcome indicators are the improvement rate of TCM syndrome, the incidence of diabetes, and the reversal rate of pre-DM. The secondary outcome indicators include fasting blood glucose, 2-hour postprandial blood glucose, glycosylated albumin, glycosylated hemoglobin, and lipid metabolism indicators. Exploratory indicators are fecal intestinal flora and branched chain amino acid (BCAA). In this study, we will observe the clinical efficacy of TDP in the treatment of prediabetic spleen deficiency and phlegm-dampness syndrome. We will evaluate its clinical value and safety, collect the plasma of the 2 groups for BCAA targeted metabolites detection, analyze differences in the gut flora-derived metabolite BCAA between the 2 groups, and explore the therapeutic mechanism of TDP in the treatment of prediabetic spleen deficiency and phlegm-dampness syndrome from the point of view of intestinal flora.

OBJECTIVE:To explore the mechanism of Tangfukang formula (, TFK) in treating type 2 diabetes mellitus (T2DM). METHODS:We employed network pharmacology combined with experimental validation to explore the potential mechanism of TFK against T2DM. Initially, we filtered bioactive compounds with the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and Symptom Mapping (SymMap), and gathered targets of TFK and T2DM. Subsequently, we constructed a protein-protein interaction (PPI) network, enriched core targets through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), and adopted molecular docking to study the binding mode of compounds and the signaling pathway. Finally, we employed a KKAy mice model to investigate the effect and mechanism of TFK against T2DM. Biochemical assay, histology assay, and Western blot (WB) were used to assess the mechanism. RESULTS:There were 492 bioactive compounds of TFK screened, and 1226 overlapping targets of TFK against T2DM identified. A compound-T2DM-related target network with 997 nodes and 4439 edges was constructed. KEGG enrichment analysis identified some core pathways related to T2DM, including adenosine 5-monophosphate-activated protein kinase (AMPK) signaling pathway. Molecular docking study revealed that compounds of TFK, including citric acid, could bind to the active pocket of AMPK crystal structure with free binding energy of －4.8, －8 and －7.9, respectively. Animal experiments indicated that TFK decreased body weight, fasting blood glucose, fasting serum insulin, homeostasis model of insulin resistance, glycosylated serum protein, total cholesterol, triglyceride, and low-density lipoprotein cholesterol, and improve oral glucose tolerance test results. TFK reduced steatosis in liver tissue, and infiltration of inflammatory cells, and protected liver cells to a certain extent. WB analysis revealed that, TFK upregulated the phosphorylation of AMPK and branched-chain α-ketoacid dehydrogenase proteins. CONCLUSION:TFK has the potential to effectively manage T2DM, possibly by regulating the AMPK signaling pathway. The present study lays a new foundation for the therapeutic application of TFK in the treatment of T2DM.

BACKGROUND:The trend of risk prediction models for diabetic peripheral neuropathy (DPN) is increasing, but few studies focus on the quality of the model and its practical application. AIM:To conduct a comprehensive systematic review and rigorous evaluation of prediction models for DPN. METHODS:A meticulous search was conducted in PubMed, EMBASE, Cochrane, CNKI, Wang Fang DATA, and VIP Database to identify studies published until October 2023. The included and excluded criteria were applied by the researchers to screen the literature. Two investigators independently extracted data and assessed the quality using a data extraction form and a bias risk assessment tool. Disagreements were resolved through consultation with a third investigator. Data from the included studies were extracted utilizing the Checklist for Critical Appraisal and Data Extraction for Systematic Reviews of Prediction Modelling Studies. Additionally, the bias risk and applicability of the models were evaluated by the Prediction Model Risk of Bias Assessment Tool. RESULTS:The systematic review included 14 studies with a total of 26 models. The area under the receiver operating characteristic curve of the 26 models was 0.629-0.938. All studies had high risks of bias, mainly due to participants, outcomes, and analysis. The most common predictors included glycated hemoglobin, age, duration of diabetes, lipid abnormalities, and fasting blood glucose. CONCLUSION:The predictor model presented good differentiation, calibration, but there were significant methodological flaws and high risk of bias. Future studies should focus on improving the study design and study report, updating the model and verifying its adaptability and feasibility in clinical practice.

Obesity-related metabolic disorders such as metabolic dysfunction-associated fatty liver disease (MAFLD), metabolic syndrome (MetS), and type 2 diabetes mellitus (T2DM) have traditionally been treated as separate conditions. This review aims to present a unified conceptual framework in which these disorders are viewed as progressive stages within a continuous and dynamic process of metabolic dysfunction. The goal is to clarify the shared mechanisms underlying this progression and to explore the clinical value of approaching them as a continuum. Insulin resistance, chronic low-grade inflammation, adipokine imbalance, and ectopic fat accumulation are common drivers across all stages of metabolic deterioration. These processes are reinforced by coordinated dysfunction in adipose tissue, liver, skeletal muscle, pancreas, and the gut microbiota. Longitudinal and genetic studies support a typical progression from individuals with obesity to MAFLD, then to MetS and T2DM, although individual trajectories vary. Certain phenotypes such as metabolically healthy individuals with obesity and normal-weight individuals with visceral adiposity illustrate the spectrum’s heterogeneity. Early dysfunction is often reversible through lifestyle or pharmacologic intervention, underscoring the importance of timely detection. Reframing obesity-associated metabolic disorders as a continuous disease process enables more accurate risk assessment, earlier intervention, and coordinated care strategies. This integrated perspective supports a shift toward mechanism-based and individualized treatment, with the potential to reduce risk and delay progression to advanced metabolic disease and its complications.

Introduction: Diabetic peripheral neuropathy (DPN) is a common complication of type 2 diabetes, characterized by high disability and mortality rates. Pain, the primary symptom of DPN, leads to increased central nervous system responsiveness and decreased pain thresholds, resulting in conditions like hyperalgesia, anxiety, and depression-collectively referred to as "central sensitization." Changes in brain structure and function are closely linked to this phenomenon but remain unclear. While functional magnetic resonance imaging (fMRI) technology can monitor brain function changes, there is limited research on the effects of interventions on these functions in patients with DPN. Yiqi Jiedu (YQJD) Decoction has been used in China to treat DPN for many years, with some studies indicating it may improve symptoms and quality of life, but there is a lack of high-quality clinical evidence, and its central mechanism of action remains unclear. Methods: This ongoing randomized, double-blind, placebo-controlled trial aims to enroll about 88 patients aged 45-75 with DPN, diagnosed with qi deficiency and blood stasis syndrome. Participants will be randomly assigned in a 1:1 ratio to either receive YQJD Granules or the placebo, with follow-up assessments at weeks 4 and 8. The primary outcomes include the Toronto Clinical Scoring System (TCSS), Michigan Diabetic Neuropathy Score (MDNS), Traditional Chinese Medicine (TCM) syndrome score, nerve conduction velocity, and fMRI changes. Secondary outcomes will assess psychological characteristics in patients and changes in serum cytokines and glucose-lipid metabolism indicators. Discussion: This study aims to evaluate the efficacy and safety of YQJD Decoction in the treatment of DPN using fMRI technology. It will analyze changes in brain regions before and after treatment, explore the cerebral effects of YQJD, and elucidate the relationship between central sensitization and brain effect patterns in the pathogenesis of DPN. The findings of this study will provide clinical evidence and mechanistic insights for the integration of TCM and Western medicine in the treatment of DPN. It is expected to reveal the central mechanisms involved in the intervention of neuropathic pain through Chinese herbal medicine. Trial registration: Chinese clinical trial registry, ChiCTR2400084649. Registered on 22 May 2024, https://www. chictr.org.cn/.

Metabolic homeostasis, essential for energy balance, is regulated by a highly integrated network involving the nervous, endocrine, and immune systems. While traditional models emphasized endocrine feedback mechanisms and autonomic nervous control, recent evidence reveals extensive cross-talk among these systems, forming a dynamic neuro-endocrine-immune network. The brain coordinates energy balance by integrating signals from peripheral organs, regulating appetite, metabolic rate, and nutrient utilization. Immune responses, particularly in obesity, contribute to metabolic dysfunction through chronic inflammation and cytokine cascades. This review synthesizes the cellular and molecular mechanisms underlying the neuro-endocrine-immune interactions that maintain glucose and energy homeostasis. We describe the functional roles of hypothalamic feeding circuits, peripheral autonomic pathways, adipokines, incretins, and immune cell subsets in metabolic tissues. We also highlight how chronic inflammation, neuroimmune signaling, and hormonal resistance contribute to homeostatic failure. Crucially, we examine emerging therapeutic strategies targeting obesity, type 2 diabetes, metabolic syndrome, and metabolic dysfunction-associated fatty liver disease—approaches that exert multi-system effects by precisely targeting key nodes within this regulatory triad. This integrative perspective not only offers novel paradigms for intervening in complex metabolic disorders but also heralds a future where decoding this network enables personalized medicine to transform clinical practice.

This article analyzed the mechanism of Huangqi Simiao Decoction(HSD)for the treatment of type 2 diabetes mellitus(T2DM).The component targets of HSD and the related disease targets of T2DM were screened through network pharmacology.The protein-protein interaction(PPI)network of intersecting targets and the drug-component-intersecting target network were constructed to screen the potential active ingredients and targets.Molecular docking was performed using AutoDock Vina software to verify the interaction between potential components and core targets.The serum was tested by ultra performance liquid chromatography-tandem mass spectrometry,and multivariate statistical analyses,such as principal component analysis(PCA)and partial least squares discriminant analysis(PLS-DA),were used to search for the differential metabolites and related metabolic pathways of each group by combining with the MetaboAnalyst database.The same metabolic pathways were analyzed by combining the screened differential metabolites with the intersecting targets screened by network pharmacology.Network pharmacology showed that the nine core components of HSD for the treatment of T2DM were quercetin,kaempferol,stigmasterol,baicalein,β-sitosterol,flavodoxin,canthaxanthin,canthaxanthin,berberine,and berberine,and the five core targets included AKT1,TP53,TNF,IL6,and VEGFA.Molecular docking showed that the core components bound well to the target genes.Metabolomics showed that a total of 112 common differential metabolites were identified,of which 88 metabolites exhibited increased concentration and 24 metabolites decreased concentration after treatment with HSD.Enrichment analysis showed that HSD regulated the body metabolism of patients with T2DM,mainly related to seven metabolic pathways,such as amino acid metabolism and tricarboxylic acid cycle.The joint analysis of metabolomics and network pharmacology showed that both involved histidine metabolism,arginine and proline metabolic pathways.This study suggests that HSD has a good efficacy for T2DM.Based on the combined analysis of metabolomics and network pharmacology,it was found that the mechanism may be that the pharmacodynamic bases of quercetin,kaempferol,and stigmasterol in HSD enhance the effects on histidine metabolism,arginine and proline metabolic pathways by modulating a variety of metabolites,which provides the basis for further prevention and treatment of T2DM.

总结在院前急救中采用针灸救治急症的经验,认为针灸具有携带方便、操作简便、价格低廉、疗效可靠、无不良反应等优点,将其应用于院前急救可减少药物的使用,为进一步救治赢得时间,且能提高急救效果、改善急症预后.通过科普宣传、培养院前急救医生等措施,加强针灸在院前急救中的应用,对提升院前急救的整体水平具有一定的现实意义.

"气虚生毒"理论认为,胃癌前病变发病源于气虚,虚气留滞导致痰、湿、热、瘀等病理产物蕴积,日久则化为诸毒,侵袭脏腑经络而致病.基于胃癌前病变虚实夹杂、毒邪纷争的病理特点,治疗应在益气培元的基础上灵活施以解毒之法,包括利解湿毒、清化痰毒、清解热毒、通化瘀毒及攻除癌毒等治法,同时应注重调肝理气,协调脾胃气机升降,使正气得扶,毒邪得除.

糖尿病前期是血糖失稳态状态过渡到糖尿病之间的高糖代谢综合征,归属于中医"脾瘅"范畴.冯兴中教授认为,脾虚肝郁、湿热内蕴为本病的核心病机,其中,脾虚为发病之本,肝郁为发病之因,湿热为发病之渐,以健脾疏肝、清热祛湿为主要治法,圆机活用自拟经验方糖抵方治疗本病,每获良效,可为中医治疗糖尿病前期提供参考价值.

文章总结临证应用四逆散合方治疗糖尿病并发症验案4则,包括四逆散合生脉散治疗糖尿病性视网膜病变、四逆散合四妙散治疗糖尿病肾病、四逆散合左金丸治疗糖尿病胃肠病变、四逆散合补阳还五汤治疗糖尿病周围血管病变,效果显著.

目的 评价龟龄集胶囊治疗轻-中度老年认知障碍(CI)肾虚髓减证的有效性和安全性.方法 本研究方案在ClinicalTrials.gov注册(ID.NCT03647384).采用多中心随机双盲对照试验的方法,将348例2018年9月—2020年9月全国13家医院收治的CI患者,按简单随机方法分为试验组和对照组,每组174例.试验组采用龟龄集胶囊(早饭前2 h淡盐水送服,2粒/次,每日1次)及银杏叶片模拟剂(1片/次,每日3次)治疗,对照组采用银杏叶片(1片/次,每日3次)及龟龄集胶囊模拟剂(早饭前2 h淡盐水送服,2粒/次,每日1次)治疗,服药疗程24周.治疗24周后,对两组疗效和安全性进行比较.主要疗效指标:简易精神状态检查表(MMSE)、蒙特利尔认知评估量表(MoCA)改善情况.次要疗效指标:阿尔茨海默病评定量表-认知项目(ADAS-Log)、日常生活能力(ADL)评分量表、中医证候评分量表改善情况,及神经递质血清乙酰胆碱(Ach)和乙酰胆碱酯酶(AchE)的含量,以及细胞凋亡因子Bax和Bcl-2的变化情况.安全性指标以不良事件发生率为主.结果 与本组治疗前比较,两组患者治疗12、24周MMSE评分、中医证候评分均升高,两组患者治疗24周ADAS-cog总评分降低(P＜0.01,P＜0.05);试验组患者治疗12、24周MoCA总评分升高(P＜0.01),24周血清Ach含量明显升高(P＜0.05);对照组治疗24周血清Bax、AchE含量降低(P＜0.05),对照组患者治疗24周MoCA总评分升高(P＜0.01),ADL总评分降低(P＜0.05).与对照组同期比较,试验组治疗24周后患者健忘、腰膝酸软证候改善有效率升高(P＜0.05).结论 龟龄集胶囊可改善CI肾虚髓减证患者认知功能,提高学习记忆能力,与银杏叶片疗效相当.

Background Imidazole Propionate (ImP) is a new marker of Type 2 diabetes mellitus (T2DM), which can induce impaired glucose metabolism and weaken the efficacy of metformin. An extensive exploration into literature suggests that ImP may be associated with stool consistency. Purpose Through an in-depth study of the relationship between stool consistency, bile acids, fecal microbiota and ImP, we intend to explore the mechanism driving the ImP content difference in T2DM. Patients Under Study and Methods This is a single-center, prospective, cross-sectional study. Plasma ImP and stool consistency were analyzed among 96 diabetic subjects and 45 healthy subjects. All subjects were divided into the stool consistency normal (N) group and the stool consistency abnormal group, of which the abnormal group was sub-divided into the hard stool (H) group and the soft stool (S) group. After identifying the correlation between ImP and stool consistency, we analyzed the influence of bile acids and fecal microbiota on ImP in diabetic subjects. Results For T2DM patients, the ImP level of the abnormal stool consistency group was significantly higher than that of the normal stool consistency group (P < 0.001). Results were verified in 45 healthy subjects (P = 0.002). ImP was significantly associated with taurocholic acid (TCA) (P = 0.003) in feces, taurodeoxycholate (TDCA) (P = 0.003), glycochenodeoxycholate (GCDCA) (P = 0.021), and glycocholic acid (GCA) (P = 0.031) in plasma. The Shannon index of Group N was significantly higher than that of Group H (P = 0.041) and Group S (P = 0.003). Conclusion ImP was higher in diabetic patients with abnormal stool consistency than in those with normal stool consistency, which was related to the proportion of bile acids and fecal microbial structure. These findings may improve our understanding of ImP and contribute to the treatment of T2DM by improving stool consistency.

帕金森病( Parkinson' s disease,PD)是中老年运动障碍性疾病中最为常见的中枢神经系统变性疾病[1] ,以静止性肢体震颤、肌肉强直、运动迟缓和姿势反射异常等运动症状为主要临床特征,常伴随便秘、睡眠障碍、汗出异常等自主神经功能紊乱以及认知功能下降等非运动症状.近年来,其发病率随着人口老龄化的增长而增加.

目的:探讨益智解毒汤治疗糖尿病大鼠认知功能障碍的作用机制.方法:制备糖尿病认知功能障碍大鼠模型,将模型大鼠按随机数表法分为糖尿病模型组,益智解毒汤低、中、高剂量组及盐酸多奈哌齐组,另设正常对照组,每组8只,给予相应药物灌胃进行干预,每日1次,连续4周.用Morris水迷宫实验测试大鼠的学习记忆能力;Western Blot检测海马组织中核苷酸结合寡聚化结构域样受体3(NLRP3)、凋亡相关斑点样蛋白(ASC)、Caspase-1、白细胞介素1 β(IL-1 β)、白细胞介素18(IL-18)蛋白表达水平;PCR检测海马组织中Bax、Bcl-2、Caspase-3 mRNA表达水平.结果:与糖尿病模型组比较,益智解毒汤高剂量组及盐酸多奈哌齐组大鼠逃避潜伏期显著缩短,穿越原平台次数显著增加(P＜0.05),益智解毒汤高剂量组显著降低海马组织中NLRP3、ASC、Caspase-1、IL-1 β、IL-18蛋白及Bax、Caspase-3 mRNA表达水平(P＜0.05,P＜0.01),显著上调Bcl-2 mRNA表达水平(P＜0.01).结论:益智解毒汤可改善糖尿病认知功能障碍大鼠的学习记忆能力,可能是通过影响NLRP3炎症通路的激活、调控细胞凋亡而发挥作用的.

Objective It is to evaluate the clinical efficacy and safety of Guilingji in the treatment of mild-to-moderate elderly cognitive impairment with kidney dificiency and marrow reduction syndrome. Methods Twenty-four elderly patients with mild-to-moderate elderly cognitive impairment with kidney dificiency and marrow reduction syndrome treated at Yuquan Hospital of Tsinghua University from May to September 2019 were selected as study subjects, and they were randomly divided into 2 groups using the random number table method, 12 cases in the experimental group were treated with Ginkgo biloba simulant+Guilingji, and the control group was treated with Guilingji simulant+Ginkgo biloba. Both groups were treated for 24 weeks. The scores of Simple Mental State Examination Scale（MMSE）, Montreal Cognitive Assessment Scale（MoCA）, Alzheimer’s Disease Assessment Scale-Cognitive Scale（ADAS-cog）, Clinical Dementia Rating Scale（CDR）, Chinese Medicine Symptom Scale, the levels of serum Bax, Bcl-2 and Bcl-2/Bax before and after treatment were compared between the two groups, and the treatment safety was observed in the two groups. Results After 12 and 24 weeks of treatment, the MMSE scores and MoCA scores in both groups were significantly higher than those before treatment（all P＜0.05）, and the scores were significantly higher in the experiment group than those in the control group after 12 weeks of treatment（all P＜0.05）. After 12 and 24 weeks of treatment, the ADAS-cog scores in both groups were significantly lower than those before treatment（all P＜0.05）, all were significantly lower after 24 weeks of treatment than those after 12 weeks of treatment（all P＜0.05）, and the experiment group was significantly lower than the control group after 12 and 24 weeks of treatment（all P＜0.05）. The CDR score was significantly lower in the experiment group after 12 weeks of treatment compared with that before treatment（P＜0.05）, and there were no statistically significant differences in the CDR scores between the 2 groups after 12 and 24 weeks of treatment（all P＞0.05）. After 12 and 24 weeks of treatment, the TCM symptom scale scores in both groups were significantly lower than those before treatment（all P＜0.05）, and both were significantly lower after 24 weeks of treatment than those after 12 weeks of treatment（both P＜0.05）, and the experiment group was significantly lower than the control group after 12 weeks of treatment（P＜0.05）. After 24 weeks of treatment, the level of serum Bcl-2 and Bcl-2/Bax ratio in the experiment group were significantly higher than those in the pre-treatment and control groups（all P＜0.05）, and the level of serum Bax was significantly lower than those in the pre-treatment and control groups（both P＜0.05）. No significant abnormal changes in blood routine, liver function and kidney function were observed during treatment in the 2 groups, and no significant adverse reactions were observed. Conclusion Compared with Ginkgo tablets, Guilingji is more effective in improving the cognitive function and improving TCM symptoms such as forgetfulness and fatigue in patients with mild-to-moderate elderly cognitive impairment with kidney deficiency and marrow reduction syndrome, its security is good. Guilingji may improve cognitive function by inhibiting cell apoptosis through Bax/Bcl-2/Caspase signaling pathway.

目的 客观评价中医综合治疗方案对糖尿病周围神经病变(气阴两虚、血脉瘀滞证)的临床疗效以及对脑源性神经营养因子(brain derived neurotrophic factor,BDNF)和胰岛素样生长因子-1(insulin-like growth fators-1,IGF-1)的影响,初步探讨其作用机制.方法 将符合诊断标准的93例糖尿病周围神经病变(气阴两虚、血脉瘀滞证)患者随机分为治疗组47例、对照组46例.在采用相同治疗的基础上,对照组给予甲钴胺,治疗组采用中药内服联合外洗综合治疗,疗程为3个月.观察两组治疗后临床疗效、多伦多临床评分系统(TCSS)评分、腓总神经、胫神经传导速度及血清BDNF和IGF-1的变化.结果 治疗后,治疗组总有效率明显高于对照组(P＜0.05);治疗组患者神经传导速度较对照组明显提高(P＜0.05);治疗组能明显增加患者血清BDNF和IGF-1的表达,差异有统计学意义(P＜0.05).结论 采用中药内服联合外洗综合治疗方案可提高糖尿病周围神经病变患者的临床疗效,其作用机制可能与增加患者BDNF和IGF-1有关.

Background: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes. Its clinical manifestation is proteinuria, and it is a common cause of renal failure. At present, angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor antagonists are often used to treat early DN, and they have good curative effect. On this basis, the treatment of early DN with the combination of astragalus injection is becoming more and more widespread. Therefore, the purpose of this study is to prove the efficacy and safety of astragalus injection combined with Western medicine in the treatment of early DN, and to provide reference value for clinical practice in the future. Methods: English databases (PubMed, Embase, Web of Science, the Cochrane Library) and Chinese databases (China National Knowledge Infrastructur, Wanfang, VP Information Chinese Journal Service Platform, China Biology Medicine disc) will be searched by computer. From the establishment of the database to February 2021, a randomized controlled trial of astragalus injection combined with Western medicine in the treatment of early DN will be conducted. Two researchers independently evaluate the quality of the included study and extract the data. Included literature is analyzed by Meta with RevMan5.3 software. Results: In this study, the efficacy and safety of astragalus injection combined with Western medicine in the treatment of early DN are evaluated by serological indexes such as Urinary albumin excretion rates (UAER), serum creatinine and blood urea nitrogen, as well as the adverse reactions of drugs. Conclusion: This study will provide reliable evidence-based evidence for astragalus injection combined with Western medicine for the treatment of early DN. OSF Registration number: DOI 10.17605/OSF.IO/A9JGP