Copper is essential for mitochondrial respiration, antioxidant defense, extracellular matrix maturation, and cellular signaling, yet disturbances in its abundance or intracellular distribution can damage the kidney through mechanistically distinct pathways. Cuproptosis is a specific copper-dependent form of regulated cell death in which copper binds lipoylated mitochondrial proteins, promotes aggregation of tricarboxylic acid cycle components, destabilizes iron-sulfur cluster proteins, and elicits FDX1- and protein lipoylation-dependent proteotoxic stress. This mechanism should be distinguished from broader copper-associated injury, including redox imbalance, glutathione depletion, respiratory-chain inhibition, senescence, apoptosis, and lysyl oxidase-mediated matrix remodeling. This narrative review examines how renal copper uptake, trafficking, and compartmentalization interact with cell-specific metabolism to shape copper-related cell fates across acute kidney injury, nephrotoxicity, renal ischemia-reperfusion injury, crystal- and lipid-related tubular injury, diabetic kidney disease, podocyte injury, chronic kidney disease and renal fibrosis, end-stage renal disease, renal cell carcinoma, and hereditary copper disorders. Mechanistic evidence is strongest in selected acute tubular, crystal-injury, and renal cancer models, in which transporter manipulation, DLAT oligomerization, iron-sulfur perturbation, or functional rescue has been demonstrated. In chronic kidney disease and fibrosis, copper-DLAT interactions, complex IV inhibition, COMMD1-SOD1 dysfunction, and ATP7A-FBLN4-LOX signaling establish pathogenic copper dependence but do not yet demonstrate a complete canonical cuproptosis pathway. By integrating disease-specific evidence with the molecular determinants of copper handling and protein lipoylation, this review identifies current therapeutic opportunities, candidate biomarkers, and key research priorities while preserving the distinction between cuproptosis and other forms of copper-associated kidney injury.

BackgroundScalp, nail, and palmoplantar psoriasis are termed “difficult-to-treat sites” owing to their unique anatomical features and therapeutic resistance, substantially impairing patient quality of life. Although anti-IL-17 and anti-IL-23 biologics are widely used, head-to-head comparative evidence for achieving high-level lesion clearance at these specific sites remains limited.MethodsFollowing PRISMA-NMA guidelines, we systematically searched PubMed, Embase, and other databases from inception through November 2025 for randomized controlled trials (RCTs). Primary outcomes were defined as complete or near-complete clearance. Frequentist network meta-analysis was performed to calculate odds ratios (ORs), with treatment rankings derived from surface under the cumulative ranking curve (SUCRA) values.ResultsTwenty-four RCTs involving 5,946 patients and eight biologics plus placebo were included. For palmoplantar psoriasis, secukinumab ranked highest (SUCRA = 79.7%), followed by bimekizumab (72.2%) and ustekinumab (69.7%). For nail psoriasis, bimekizumab ranked first (78.9%), followed by ixekizumab (77.2%) and brodalumab (67.5%); however, local inconsistency for the ixekizumab–placebo comparison and low-certainty evidence warrant caution. For scalp psoriasis, brodalumab (87.7%) and ixekizumab (86.9%) ranked highest, followed by bimekizumab (69.0%) and guselkumab (65.1%); the brodalumab estimate relied on a single contributing study.ConclusionDuring induction-phase follow-up, IL-17 inhibitors tended to rank highly for complete or near-complete clearance at difficult-to-treat psoriasis sites. Bimekizumab and ixekizumab showed consistently favorable rankings across sites, but treatment selection should consider certainty of evidence, sensitivity analyses, long-term response, and patient-level factors.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO, identifier CRD420251271255.

Iron (Fe), copper (Cu), and zinc (Zn) are essential trace elements for cardiovascular and cerebrovascular homeostasis, acting as enzymatic cofactors in energy metabolism and antioxidant defence. However, disruption of metal homeostasis can amplify oxidative injury through direct Fe/Cu redox chemistry or indirect Zn-dependent pathways. Ferroptosis and cuproptosis have been investigated as context-dependent mechanisms in various cardiovascular and cerebrovascular diseases (CCVDs), such as atherosclerosis, ischaemic/haemorrhagic stroke, diabetic vascular disease, and abdominal aortic aneurysm. This review summarizes the physiological regulation of metal homeostasis and examines pathways through which metal dyshomeostasis may contribute to vascular and neural injury, including oxidative biomolecular modification, mitochondrial dysfunction and inflammatory signalling. It further summarizes therapeutic strategies targeting metal metabolism, such as metal chelators, trace element supplementation and nanomedicine-based targeted delivery systems, which have shown protective effects predominantly in experimental models by restoring metal homeostasis and scavenging reactive oxygen species. Finally, the review highlights key challenges in clinical translation, such as tissue-specific metal detection and targeted inhibitor development, and emphasizes that precise regulation of metal metabolism may offer therapeutic opportunities for CCVDs.

BackgroundLong-term use of conventional therapy (CT) for psoriasis vulgaris (PV) is often constrained by adverse effects and costs. While oral plant-derived bioactive compounds show clinical promise as adjunctive treatments, the relative efficacy and safety of these compounds and their combination regimens remain poorly defined due to a lack of head-to-head comparisons. This systematic review and network meta-analysis aimed to compare and rank the efficacy and safety of different oral plant-derived bioactive compounds and their combination regimens for PV.MethodsRandomized controlled trials investigating the effects of plant-derived bioactive compounds, such as compound glycyrrhizin (CG), tripterygium glycosides (TG), and total glucosides of paeony (TGP), on PV were retrieved from Chinese and English databases via computer searches. The main outcome measures included the Psoriasis Area and Severity Index (PASI), CD4+/CD8+ ratio, IL-23, IL-17, and TNF-α. Network meta-analysis was performed using Stata 16.0 software.ResultsWe included 84 randomized controlled trials comprising 7,544 patients across 15 treatment regimens. Most combination therapies significantly outperformed monotherapy in PASI reduction. TG combined with topical therapy (TOP) produced the greatest reduction in PASI scores [mean difference (MD) = −13.96, 95% confidence interval (CI) (−16.88, −11.03)], with the highest surface under the cumulative ranking curve (SUCRA) value of 99.80%. Individual compounds showed distinct advantages for specific therapeutic targets. CG + TOP proved most effective for reducing IL-23 levels (SUCRA = 97.30%), while CG + NB-UVB achieved the greatest IL-17 reduction (SUCRA = 91.20%). CG + CT best restored CD4+/CD8+ ratio balance (SUCRA = 94.70%), and TGP + TOP led all regimens in TNF-α suppression (SUCRA = 92.40%). Adverse events were predominantly mild, consisting of gastrointestinal symptoms or skin dryness. No serious or irreversible events were recorded.ConclusionCombining plant-derived compounds with CT may enhance short-term, outcome-specific efficacy. TG + TOP showed the greatest PASI reduction. Immunologically, CG-based regimens optimized IL-23/IL-17 suppression and CD4+/CD8+ normalization, while TGP + TOP maximized TNF-α inhibition. These distinct profiles inform individualized treatment and warrant long-term confirmation.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261304681, identifier (CRD420261304681).

Ethnopharmacological relevance Chronic fatigue syndrome (CFS) is a chronic intractable disease, displaying abnormal energy metabolism, resulting in significant energy deficiency. Shengyang Sanhuo Decoction (SYSH), with its exquisite compatibility of traditional Chinese medicine (TCM), has been clinically used for treating CFS. However, its pharmacological mechanisms remain underexplored. Aim of the study To analyse the therapeutic effects of SYSH and its disassembled prescriptions (Group A: Qi-tonifying; Group B: Wind-dispelling) on CFS, with a focus on autophagy function and lipid metabolism. Methods A multi-stress-induced CFS mouse model was established. Behavioural assessments, transmission electron microscopy, serum biochemistry, and western blot were performed to evaluate the regulation of autophagy and energy homeostasis. Chemical composition was analysed using LC-MS/MS, and mechanisms elucidated through integrated network pharmacology and lipidomics. Results SYSH, Group A, and Group B significantly ameliorated fatigue-like behaviours and reduced serum biomarkers, including lactate dehydrogenase (LDH), creatine kinase (CK), and blood urea nitrogen (BUN). Treatments elevated adenosine triphosphate (ATP) levels and modulated the autophagy signalling pathway to promote autophagosome-lysosome formation. Crucially, Group A predominantly restored phospholipid (PC/PE), while Group B primarily modulated the sphingolipid (ceramide/S1P) rheostat. Conclusions SYSH and its disassembled prescriptions alleviated CFS by regulating lipid metabolism: Qi-tonifying herbs preferentially enhance phospholipid availability, while wind-dispelling herbs more prominently restore sphingolipid homeostasis, supporting the TCM formula compatibility theory.

Objective:In this study, we investigated the potential mechanism of action of Qing Bi Yin (QBY) in psoriasis treatment via regulation of the sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptor 1 (S1PR1) pathway and Th17 cell differentiation. Methods:Network pharmacology was used to identify potential targets and elucidate the potential mechanisms of QBY in psoriasis. The predicted mechanisms were validated with in vitro Th17 cell differentiation assays using isolated mouse splenic CD4+ T cells. Molecular docking was performed to evaluate the binding affinities between active compounds and key target proteins. Results:We identified 262 overlapping QBY psoriasis target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed significant associations with the sphingolipid signaling pathway, Th17 cell differentiation, and IL-17 signaling pathway. Network algorithms were used to identify 10 key active compounds and five hub genes. QBY treatment suppresses S1P synthesis and S1pr1 expression in Th17-polarized cells. QBY inhibited Th17 cell proliferation and differentiation, reduced inflammatory cytokine secretion by Th17 cells via the S1P/S1PR1 pathway, and modulated STAT3 and SMAD2 phosphorylation. Molecular docking showed strong binding affinities between active compounds (glabridin, luteolin, licoflavone A, and isobutyrylshikonin) from QBY and key targets (STAT3, SMAD2, SPHK1, and RORγt) in Th17 cells. Conclusion:QBY ameliorates psoriatic inflammation by regulating Th17 cell differentiation via the S1P/S1PR1 signaling pathway. These findings underscore the clinical translational potential of QBY and its active constituent glabridin.

Phlorizin (PHZ) is a glucoside of phloretin, belonging to the dihydrochalcone class within flavonoids; It is one of the active ingredients of the plant Cynomorium, and it has been shown that PHZ can regulate lipid metabolism disorders as well as having anti-aging properties. However, no studies have investigated whether PHZ ameliorates Aβ-induced toxicity in Alzheimer’s disease (AD) by regulating fatty acid β-oxidation. This study aims to investigate the effects of PHZ on the regulation of fatty acid β-oxidation and resistance to Aβ-associated toxicity on the AD Caenorhabditis elegans and the mechanisms of action. Wild-type N2 and AD model CL4176 C. elegans were used; lifespan, heat stress resistance, chronic paraquat stress, reactive oxygen species (ROS), behavioral performance, and lipofuscin accumulation assays were examined to evaluate the anti-aging effects; and non-esterified fatty acid (NEFA), triglyceride (TG) and lipidomic contents were quantified after PHZ treatment. The detection of genes related to fatty acid β-oxidation pathways was performed using qRT-PCR. nhr-49 knockout mutant RB1716; and GFP-binding mutants PMD150 WBM170 were used to observe the effect of PHZ on NHR-49 pathways, and molecular docking studies were performed by combining PHZ with NHR-49 proteins. Results showed that PHZ improved worms’ survival and delayed senescence, as demonstrated by enhanced performance in lifespan, heat stress, ROS, and paraquat assays and chronic paraquat assays; PHZ also reduced lipid accumulation in worms, affected the unsaturated fatty acid pathway, and significantly increased the expression of fatty acid metabolism-related genes nhr-49, acs-2, and cpt-5, and can be tightly coupled to NHR-49 targets. PHZ may play an anti-Aβ toxicity role by regulating lipid metabolism disorders through the NHR-49—related pathway and anti-aging in AD worms.

Central lipid metabolism disorders are crucial for the development of Alzheimer’s disease (AD). Phlorizin (PHZ) improved lipid metabolism abnormalities in AD nematodes, but its mechanism of action in improving AD-related symptoms and whether it can alleviate AD cognitive impairment remain unclear. To elucidate the effects and mechanisms of PHZ on lipid metabolism disorders in an AD model, gavage administration of PHZ for 8 weeks improved cognitive dysfunction and lipid disorders in APPswe/PSEN1dE9 (APP/PS1) mice. Concurrently, in astrocytes induced by palmitic acid (PA)- mediated lipid metabolic disorder, PHZ treatment improved astrocytic lipid accumulation by upregulating the target peroxisome proliferator-activated receptor α (PPARα) and its downstream pathways, thereby promoting astrocytic fatty acid oxidation. We validated PHZ’s strong in vitro binding affinity with PPARα. Co-culture systems of lipid-metabolically disordered astrocytes and neurons further demonstrated that PHZ significantly improved neuronal cell viability and reduced intracellular lipid accumulation, thereby decreasing the expression of enzymes associated with β-amyloid protein (Aβ) production. This study demonstrates that gavage administration of PHZ for 2 months improves cognitive deficits and pathological markers in AD mice. Furthermore, at the cellular level, PHZ may exert its effects by enhancing astrocytic lipid metabolism, thereby preventing neuronal lipotoxicity and mitigating AD progression.

We present a case of rosacea recurrence in a 37-year-old woman associated with the intake of compound vitamin tablets during the preconception period, with a Naranjo score of 7. These tablets, commonly used for nutritional supplementation to prevent anemia, contain a variety of vitamins, minerals, and trace elements. Despite their widespread use, reports of such supplements causing rosacea recurrence are rare. In this case, the patient experienced a recurrence of facial redness, stinging, and burning after taking the tablets on two separate occasions. Skin dermatoscopy, VISIA imaging, Clinician's Erythema Assessment (CEA), Investigator's Global Assessment (IGA), and Visual Analogue Scale (VAS) all confirmed the recurrence of rosacea. Given her intention to conceive, symptomatic treatment with emollient and reparative dressings was administered. The patient's symptoms gradually resolved after discontinuing the medication, with no recurrence observed during follow-up visits. Women with a history of rosacea should avoid these tablets during preconception, pregnancy, and lactation to prevent recurrence and should choose supplements carefully to minimize the risk of rosacea flare-ups.

Background: Depression is associated to gut microbiota imbalance. Our research examined the antidepressant potential of phlorizin (PHZ), a natural anti-inflammatory compound that influences gut microbiota, and explored its underlying mechanisms. Methods: A corticosterone (CORT)-induced depression mouse model was used for evaluating the ameliorative influences of PHZ on depressive phenotypes and central neuroinflammation through behavioral tests and biochemical assays. 16S rRNA sequencing and metabolomics were used to evaluate gut microbiota composition and metabolite levels in serum and hippocampal tissue, respectively. Spearman correlation and broad-spectrum antibiotic cocktail (ABx) treatment experiments verified the effect of gut microbes in the PHZ-mediated modulation of key metabolites. A lipopolysaccharide (LPS)-induced BV2 microglial inflammation model was established to evaluate the role of metabolites in PHZ’s antineuroinflammatory effects. Results: PHZ significantly alleviated depressive-like behaviors in CORT mice and suppressed hippocampal neuroinflammation by modulating microglial M1/M2 polarization. Furthermore, PHZ altered gut microbiota composition, influenced serum methionine (Met) metabolism, and significantly increased hippocampal L-methionine (L-Met) and S-adenosylmethionine (SAMe) levels. Cellular experiments confirmed that L-Met plays a critical role in PHZ-mediated antineuroinflammatory effects. Significant correlations were observed between Parabacteroides, Parasutterella, and Alistipes and serum Met levels. ABx treatment suppressed the increase in hippocampal L-Met levels, suggesting that PHZ regulates methionine metabolism via the microbiota. These findings indicate that PHZ alleviates depressive states in CORT mice by modulating the microbiota–gut–brain axis. Conclusions: PHZ modulates the gut microbiota (namely Parabacteroides, Parasutterella, and Alistipes) and increase L-Met and SAMe levels, thereby suppressing neuroinflammation and improving depressive phenotypes in mice.

OBJECTIVE:Prenatal stress has been proven to be associated with dysbiosis of the gut microbiota. Despite the established phenomenon that psychological stress can be transmitted to offspring and the ability of maternal gut microbiota to colonize the offspring's gut through vertical transmission, the intricate relationships linking cross-generational depression with the microbiome remain poorly understood. METHODS:We utilized combined fear stress stimuli to establish a pregnancy psychological stress (PPS) rat model, in which offspring exhibited trans-generational depression-like behavior. The relationship between vertical transmission of the gut microbiome, intergenerational effects, and psychological stress in offspring was investigated using microbiology and metabolomics. RESULTS:We demonstrated that the vertical transmission of co-altered species from PPS dams to their puberty offspring was strongly associated with dysbiosis of the gut microbiota in the offspring. In terms of microbial function, both PPS dams and their offspring exhibited upregulation of glycine, glutamate, and serine metabolism in fecal samples, as revealed by untargeted metabolomics. Additionally, this microbial trans-generational effect was reflected in the prefrontal cortical tissue of PPS offspring, where serine in the pathway and its interconverted glycine was significantly increased. Furthermore, the co-altered species and metabolites of the pathway formed a highly correlated module with disordered inflammatory factors and neurotransmitters in the prefrontal cortex tissue of PPS offspring. This indicates that the microbiome plays a significant role in prefrontal cortex neuroinflammation as well as neurotransmitter disorders in depression-like offspring. CONCLUSIONS:Our findings highlight the gut microbiome as a plausible mediator of prenatal stress effects on offspring neurodevelopment, though further mechanistic validation is required.

Objective: To evaluate the effectiveness and safety of modified Xiaoyao powder for postpartum depression（PPD） by conducting a systematic review of randomized controlled trials（RCTs）.Methods: The Chinese National Knowledge Infrastructure Databases（CNKI）, the Chinese Scientific Journals Database（VIP）, Wanfang, Google Scholar, the Sino Med, Embase, Cochrane Library, and Pub Med databases were searched from their inception to April 25, 2023. The Cochrane Risk of Bias tool was used to assess the quality of the trials. We applied the risk ratio to present dichotomous data and the mean difference to present continuous data. Data with similar characteristics were pooled for meta-analysis and heterogeneity was assessed using I~2.Results: This review included 35 trials involving 2848 participants. The quality of the included studies was low（unclear randomization processes and insufficient reporting of blinding）. Participants treated with modified Xiaoyao powder plus Western medicine showed lower Hamilton Depression Scale（HAMD） depression score than those who used Western medicine alone（mean difference =-2.15; 95% confidence interval:-2.52 to 1.78; P ＜.00001）, and higher effective rate（relative risk = 1.19; 95% confidence interval: 1.15 to 1.24; P ＜.00001）, When comparing modified Xiaoyao alone with Western medicine, the HAMD depression score remained low, however, the efficacy rate was higher in the modified Xiaoyao group. Regarding adverse events, the modified Xiaoyao group reported weight gain,nausea, and diarrhea, but no severe adverse events were reported.Conclusion: Modified Xiaoyao may help relieve depression in PPD when used alone or in combination with Western medicine, with minor side effects. Therefore, future high-quality, large-sample size RCTs are warranted.

Background:Cynomorium songaricum Rupr. has long been used as an anti-inflammatory, antidepressant, and anti-aging agent in traditional Chinese medicine in Asia. Its ethyl acetate extract (ECS) has been identified as the main antioxidant component with neuroprotective and estrogen-like effects. However, the potential of ECS in treating depression has not been explored yet.Methods: We identified the primary metabolites in ECS in this study using liquid chromatography-electrospray tandem mass spectrometry (LC-MS/MS). Network analysis was used to find the potential targets and pathways associated with the anti-neuroinflammatory depression action of the ECS. In addition, we established a corticosterone (CORT)-induced depression mouse model to assess ECS’s antidepressant effects by monitoring various behavioral changes (e.g., sucrose preference, forced swimming, tail suspension, and open field tests) and biochemical indices of the hippocampus, and validating the network analysis results. Significant pathways underwent verification through western blotting based on network analysis prediction.Results: Our study demonstrates that ECS possesses significant antidepressant activity. The LC-MS/MS analysis of ECS identified 30 main metabolites, including phloridzin, phlorizin, ursolic acid, and naringenin, as well as other flavonoids, terpenoids, and phenolic acids. These metabolites were found to be associated with 64 candidate target proteins related to neuroinflammatory depression from the database, and ten hub proteins were identified through filtration: CXCL8, ICAM1, NOS2, SELP, TNF, IL6, APP, ACHE, MAOA and ADA. Functional enrichment analyses of the candidate targets revealed their primary roles in regulating cytokine production, inflammatory response, cytokine activity, and tumor necrosis factor receptor binding. In vivo, ECS improved hippocampal neuroinflammation in the mouse model. Specifically, ECS reduced the expression of inflammatory factors in the hippocampus, inhibited M1 microglial cell polarization, and alleviated depression through the regulation of the NF-κB-NLRP3 inflammation pathway.Conclusion: Based on experimental and network analysis, this study revealed for the first time that ECS exerted antidepression effect via anti-neuroinflammation. Our research provides valuable information on the use of ECS as an alternative therapeutic approach for depression.

目的 基于PPI网络探讨新型冠状病毒(SARS-CoV-2)受体ACE2在高血压靶点中的网络关联影响及相互作用关系,为临床治疗COVID-19合并高血压提供理论参考.方法 从GeneCards、DisGnet、OMIM和TTD数据库检索高血压靶点,通过关联分数筛选重要靶点,将所得靶点统一导入String平台,得到蛋白相互作用(PPI)网络,利用Cytoscape3.8.0筛选与ACE2最为直接相关的靶点后,再次通过String数据库获取新的PPI网络,提取该网络中的核心蛋白功能模块,并完成GO、KEGG富集分析.参考ACE2在各模块中的评分结果,分析其在整体网络结构中的影响意义和关联.结果 最终从高血压靶点中筛选得到33个与ACE2直接相关的蛋白,通过聚类分析发现它们共聚集形成了3个功能模块,主要涉及的生物学功能是管径调节、激素水平调节与内分泌调节,分子功能分别是执行调控受体调节子活性、外肽酶活性与激素活性,而主要富集的通路有神经活性配体受体相互作用、肾素-血管紧张素系统信号转导途径等.评分结果显示,ACE2所在模块内评分较高的是ACE2、CAT、DPP4、ACHE、CMA1,提示它们对其他蛋白模块的影响可能更大;而在跨模块关联分析中则发现AGT、AGTR1、EDN1、ALB与AGTR2评分较高,说明上述蛋白可能是模块3与其他模块发生相互作用的关键节点.结论 ACE2在高血压靶点网络中占据重要地位,而RAS是连接COVID-19与高血压病的核心枢纽,其失衡是引起单纯COVID-19患者发生血压升高或COVID-19合并高血压出现高致死率的关键所在.ACE2通过与CAT、ACHE、CMA1、EDN1等蛋白的交互作用参与升高血压,同时与COVID-19相联系,但其上调是否有助于SARS-CoV-2入侵以及ACEI、ARB类在合并高血压的COVID-19患者的应用仍有待验证.

Objective:To analyze the medication law of external application of TCM in the treatment of psoriasis vulgaris (PV) by using data mining method.Methods:Clinical controlled trial literature about external application of TCM in the treatment of PV was retrieved from CNKI, VIP, WanFang, SinoMed, PubMed and Cochrane Library from the establishment of the databases to May 23, 2022. Prescriptions were extracted after screening. TCM inheritance computing platform V3.0 was used to analyze the property, taste, meridian, efficacy, use frequency, common medicinal pairs and the core combinations.Results:A total 186 prescriptions were included, involving 190 kinds of Chinese materia medica. The medicines were mostly bitter and cold in property and taste, mainly belonging to the liver and heart meridians. Heat-clearing drugs were mainly used, followed by blood circulation-activating and stasis-eliminating medicines, and tonic medicines. The ten most frequently used medicines were Sophorae Flavescentis Radix, Dictamni Cortex, Phellodendri Chinensis Cortex, Kochiae Fructus, Angelicae Sinensis Radix, Salviea Miltiorrhizae Radix et Rhizoma, Poria, Rehmannine Radix, and Arnebiae Radix; the 3 commonly used medicinal pairs were Sophorae Flavescentis Radix- Dictamni Cortex, Sophorae Flavescentis Radix- Cnidii Fructus, and Sophorae Flavescentis Radix- Kochiae Fructus; 4 combinations were obtained through evolution. Conclusions:External application of TCM for the treatment of PV is around the core pathogenesis of "heat toxin", mainly treating from the blood, including cooling blood and detoxifcation, activating blood circulation and removing stasis, nourishing the blood and moistening dryness. Clearing heat and drying dampness, dispelling wind and relieving itching are also valued. The treating thoughts can provide some references for clinical treatment.

Objective: To investigate the bioactive components of Sangqi Qingxuan formula（SQQX）, predict the pharmacological targets, and explore the mechanism of hypertensive vascular remodeling（HVR）.Methods: Network pharmacology was adopted to predict how SQQX acts in HVR. The effectiveness was assessed by blood pressure measurements and pathological morphology observation based on a spontaneously hypertensive rat model, while the mechanism of SQQX on HVR was validated by immunohistochemistry（IHC） and western blot（WB） according to the results of network pharmacology.Results: There were 130 bioactive components of SQQX and 231 drug targets predicted by the Traditional Chinese Medicine Systems Pharmacology Database. Subsequently, 181 common targets were identified for SQQX against HVR, with TP53, MAPK1, and AKT1 as the core targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses was employed to identify the top 20 enriched functions and the top 20 pathways（P ＜.01）. Finally, the key role of the ERK/MAPK signaling pathway in HVR was determined. The in vivo results suggested that SQQX reduced systolic blood pressure and increased the ratio of thoracic aortic wall thickness to lumen diameter. Additionally, compared with the model group, SQQX increased the expression of smooth muscle 22 alpha（IHC: P ＜.001; WB:P ＜.05） and decreased the expression of osteopontin（IHC: P ＜.001; WB: P ＜.05）, ERK1/2（IHC: P ＜.001;WB: ERK1 ＆ ERK2, all P ＜.05）, p-ERK1/2（IHC: P ＜.001; WB: ERK1 ＆ ERK2, all P ＜.05）, and the ratio of pERK1/2 to ERK1/2 protein（IHC: P ＜.001）.Conclusions: SQQX, which has multiple bioactive ingredients and potential targets, is an effective treatment for HVR. The mechanism of antihypertensive and vascular protection may be related to the inhibition of phenotypic transformation of vascular smooth muscle cells and the ERK/MAPK signaling pathway.

基于中医经典理论,从心主血脉而通神明、心为君火以镇阴邪、心损不复须和营卫等角度出发,结合现代研究及临床经验,系统阐述桂枝茯苓丸治疗心系疾病的理论基础及临床应用体会.认为心主血脉,内通神明,"神明之心"与"血脉之心"异常所致的形神合病是慢性心系疾病的重要特征.桂枝茯苓丸既可化瘀,又兼安神,具有双心同调之功.心系疾病,若久虚不复,血脉壅塞,可发展为心损."损其心者,调其营卫",桂枝茯苓丸通过调和营卫、畅达血气的方式,达到气血资生、经脉通畅、伏邪外透之效,则心损可复.灵活化裁桂枝茯苓丸,可更好地发挥其活血通脉、宁心安神、温阳利水、调和营卫之功,以适用于多种复杂性心系疾病的治疗.

目的 探讨根皮苷对秀丽隐杆线虫寿命的影响.方法 ①急性热应激筛选实验:取秀丽隐杆线虫,分为空白组、0.1 mg/mL根皮苷组、0.5 mg/mL根皮苷组、1 mg/mL根皮苷组.除空白组外,其余组加入相应浓度的根皮苷干预24 h后放入35℃恒温箱中观察,统计秀丽隐杆线虫在急性热应激条件下的生存时间.②寿命实验:取秀丽隐杆线虫,分为空白组、0.05 mg/mL根皮苷组、0.1 mg/mL根皮苷组、0.2 mg/mL根皮苷组,除空白组外,其余组加入相应浓度的根皮苷干预,统计各组秀丽隐杆线虫的平均寿命.③应激实验:实验分组同寿命实验,分别进行急性热应激、过氧化氢应激和百草枯氧化应激干预,统计各组秀丽隐杆线虫生存时间.④生殖能力实验:实验分组同寿命实验,统计各组秀丽隐杆线虫产卵量和总产卵时间.结果 ①在急性热应激条件下,0.1 mg/mL根皮苷组秀丽隐杆线虫的生存时间明显长于空白组(P＜0.05),0.5 mg/mL根皮苷组、1 mg/mL根皮苷组秀丽隐杆线虫的生存时间与空白组比较差异均无统计学意义(P均＞0.05).②0.05 mg/mL根皮苷组、0.1 mg/mL根皮苷组秀丽隐杆线虫的平均寿命均明显长于空白组(P均＜0.05),0.2 mg/mL根皮苷组秀丽隐杆线虫的平均寿命与空白组比较差异无统计学意义(P＞0.05).③在急性热应激和百草枯氧化应激条件下,0.1 mg/mL根皮苷组秀丽隐杆线虫的生存时间均明显长于空白组(P均＜0.05),0.05 mg/mL根皮苷组、0.2 mg/mL根皮苷组秀丽隐杆线虫的生存时间与空白组比较差异均无统计学意义(P均＞0.05);在过氧化氢应激条件下,空白组、0.05 mg/mL根皮苷组、0.1 mg/mL根皮苷组、0.2 mg/mL根皮苷组线虫的生存时间比较差异均无统计学意义(P均＞0.05).④0.05 mg/mL根皮苷组、0.1 mg/mL根皮苷组、0.2 mg/mL根皮苷组秀丽隐杆线虫的产卵量和总产卵时间与空白组比较差异均无统计学意义(P均＞0.05).结论 根皮苷能够提高秀丽隐杆线虫的抗应激能力,延长其平均寿命,但不影响其生殖能力.

阐释通降阳明法在高血压病中的应用规律.通降阳明法即通过除壅、降气等方式,使阳明恢复和降之本性,从而处理高血压"厥阴上干,久则阳明失降"的相关病症.从经典理论出发,归纳通降阳明的具体方法有四:一是通腑泄热法,为阳明之正治,适用于阳明热实证,代表方如大柴胡汤,代表药有大黄、决明子等;二是涤痰消食法,扫清阳明之垢浊,适用于痰湿食滞证,代表药有莱菔子、全瓜蒌、旋覆花等;三是濡养胃阴法,养胃体以降阳明,适用于胃阴亏虚证,代表方如一贯煎;四是肃降肺金法,肃肺金以降阳明,适用于肺金壅塞证,代表方如苏子降气汤,代表药有苦杏仁、紫菀等.