Journal of Traditional and Complementary Medicine最新文献_第8页

Analyzing mechanisms of qing fei bao yuan decoction granules in treating COPD based on LC-MS, network pharmacology and in vivo methods 基于LC-MS、网络药理学和活体方法分析清热保元颗粒治疗慢性阻塞性肺疾病的机制

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-05-01 Epub Date: 2024-04-14 DOI: 10.1016/j.jtcme.2024.04.005

Amei Tang , Yang Liu , Guoqiang Guan , Tong Hao , Feng Cao

Background and aim

The current therapeutic interventions of chronic obstructive pulmonary disease offer only partial alleviation of symptoms, leaving the majority of patients with persistent and significant clinical manifestations. This investigation seeks to elucidate the underlying pharmacological mechanisms of Qing Fei Bao Yuan Decoction (QFBYD) employing a multidisciplinary approach that includes network pharmacology and molecular docking techniques.

Experimental procedure

The QFBYD formulation were subjected to mass spectrometry analysis, while critical compounds and biological targets were subsequently identified through the TCMSP database. Disease- and drug-specific targets were collated from a plethora of databases, including Batman-TCM, Stitch, Swiss Target Prediction and GeneCards. GO and KEGG pathways were analyzed for the collected targets. A PPI network was constructed using STRING database to isolate core targets. Molecular docking was executed using Auto Dock Tools and PyMOL software, and an animal model of COPD was developed for experimental validation.

Results and conclusions

Seven salient compounds and five core biological targets were ascertained through our analysis. Additionally, four compounds demonstrated high-affinity binding to the identified targets. Pathways involving bacterial endotoxin response, oxidative stress regulation, and endothelial cell migration were significantly enriched according to the KEGG database. Animal models substantiated that QFBYD ameliorated pathological hallmarks, enhanced respiratory functionality, mitigated overexpression of pro-inflammatory cytokines, augmented the antioxidant defense mechanism, and suppressed the hyperactivity of the five core targets. The efficacy of QFBYD in COPD treatment may be primarily attributed to its role in moderating inflammatory responses and rectifying oxidative imbalances.

背景和目的目前慢性阻塞性肺疾病的治疗干预措施只能部分缓解症状，使大多数患者具有持续和显著的临床表现。本研究旨在通过网络药理学和分子对接技术等多学科方法，阐明清肺保元汤的潜在药理机制。实验程序QFBYD制剂进行质谱分析，随后通过TCMSP数据库鉴定关键化合物和生物靶点。疾病和药物特异性靶标是从大量数据库中整理出来的，包括Batman-TCM、Stitch、Swiss Target Prediction和GeneCards。对收集到的靶点进行GO和KEGG通路分析。利用STRING数据库构建PPI网络，分离核心目标。使用Auto Dock Tools和PyMOL软件进行分子对接，并建立COPD动物模型进行实验验证。结果与结论通过分析确定了7个突出化合物和5个核心生物学靶点。此外，四种化合物与鉴定的靶标表现出高亲和力结合。根据KEGG数据库，涉及细菌内毒素反应、氧化应激调节和内皮细胞迁移的途径显著丰富。动物模型证实，QFBYD改善了病理标志，增强了呼吸功能，减轻了促炎细胞因子的过度表达，增强了抗氧化防御机制，并抑制了五个核心靶点的过度活性。QFBYD在COPD治疗中的疗效可能主要归因于其调节炎症反应和纠正氧化失衡的作用。

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引用次数: 0

Curcumol promotes ferroptosis of colon cancer by targeting the ubiquitination and degradation of GPX4 姜黄醇通过靶向 GPX4 的泛素化和降解促进结肠癌的铁变态反应

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-08-21 DOI: 10.1016/j.jtcme.2024.08.006

Wuxia Zhao , Qiuying Yan , Lianfang Liu , Dahai Hou , Dongyang Xiang , Dongxin Tang , Liu Li , Weixing Shen , Weiwei Tao , Haibo Cheng , Dongdong Sun

Background and aim

Colon cancer (CC) is one of the common malignant tumors in the digestive tract, the prognosis of CC patients has never been satisfying. A Ferrous-dependent form that regulates cell death, plays a key role in cancer development. As a core regulator of ferroptosis, GPX4 has become a potential molecular target for the development of antitumor drugs. Curcumol (Cur), a sesquiterpene natural product, it has significant anti-tumor effect. However, whether Cur mediates ferroptosis in colon cancer and its mechanism are still unclear. This study aimed to investigate the underlying mechanisms of Cur anti-tumor.

Experimental procedure

By investigating the Cancer Genome Atlas (TCGA) database and tissue immunofluorescence staining was also used to detect the levels of GPX4 protein in CC and matching paracancerous tissues. The anti-CC and pro-ferroptosis effects of Cur were detected in the vivo and vitro experiment. The interaction between Cur and GPX4 was predicted. In addition, the potential mechanism of Cur anti-CC was further discussed. Co-immunoprecipitation was used to confirm Cur-mediated GPX4 ubiquitination.

Results and conclusion

GPX4 was upregulated in CC tissue and was correlated with poor survival of patients. Cur inhibited the proliferation of CC cells, accompanied by regulating Fe²⁺ overload, reactive oxygen species (ROS) formation, malondialdehyde (MDA) production and superoxide dismutase (SOD) consumption. Furthermore, GPX4 was predicted and verified as the direct target of Cur by molecular docking and structure-based virtual prediction. Meanwhile, Cur could promote the ubiquitination-mediated degradation of GPX4, induce ferroptosis in CC cells and regulate the expression of ferroptosis-related protein FTH1 and TfR1. In addition, when GPX4 was overexpressed (GPX4-OE), the inhibitory effect of Cur on the expression of GPX4 and ferroptosis-related protein FTH1 and the promotion of TfR1 expression were abolished. Cur could inhibit CC by increasing the ubiquitination degradation level of GPX4 to induce ferroptosis in CC cells.

背景与目的结肠癌（colorectal cancer， CC）是消化道常见的恶性肿瘤之一，其预后一直不理想。一种调节细胞死亡的铁依赖形式在癌症发展中起着关键作用。GPX4作为铁下垂的核心调控因子，已成为开发抗肿瘤药物的潜在分子靶点。Curcumol （Cur）是一种倍半萜类天然产物，具有显著的抗肿瘤作用。然而，Cur是否介导结肠癌铁下垂及其机制尚不清楚。本研究旨在探讨其抗肿瘤作用机制。通过肿瘤基因组图谱（Cancer Genome Atlas， TCGA）数据库和组织免疫荧光法检测GPX4蛋白在CC及配对癌旁组织中的表达水平。在体内和体外实验中检测了Cur的抗cc和促铁下垂作用。预测了Cur与GPX4的相互作用。此外，还进一步探讨了氯化铜抗氯化铜的潜在机理。共免疫沉淀法证实了curr介导的GPX4泛素化。结果与结论ongpx4在CC组织中表达上调，与患者生存不良相关。Cur抑制CC细胞增殖，同时调节Fe2+过载、活性氧（ROS）形成、丙二醛（MDA）产生和超氧化物歧化酶（SOD）消耗。通过分子对接和基于结构的虚拟预测，预测并验证了GPX4是Cur的直接靶点。同时，Cur可促进泛素化介导的GPX4降解，诱导CC细胞铁沉，调节铁沉相关蛋白FTH1和TfR1的表达。此外，当GPX4过表达（GPX4- oe）时，Cur对GPX4和铁凋亡相关蛋白FTH1表达的抑制作用以及对TfR1表达的促进作用被取消。Cur可以通过提高GPX4的泛素化降解水平来抑制CC，诱导CC细胞铁凋亡。

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引用次数: 0

Guilingji capsules enhances erectile function by promoting testosterone-dependent angiogenesis in the corpus cavernosum 龟苓姬胶囊通过促进海绵体中睾酮依赖性血管生成而增强勃起功能

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-06-18 DOI: 10.1016/j.jtcme.2024.06.009

Xujun Yu , Jingyi Zhang , Suyun Xu , Jing Zhou , Chenglin Zhuang , Junjun Li , Baojun Zhuang

Background and aim

Guilingji capsules (GLJC) have the effect of treating erectile dysfunction (ED). This study aims to explore the potential mechanisms of GLJC in treating ED.

Experimental procedure

We conducted network pharmacology analysis of ED-related targets with GLJC components reported in the TCMSP database and GLJC components reported in the literature, respectively. Molecular docking was employed to validate the binding affinity of these molecular targets. Animal experiments were conducted to validate the aforementioned results. The mechanism of GLJC in treating ED was studied using d-galactose-induced aging rats, and orchiectomized rats were used to investigate further whether the mechanism of GLJC in treating ED is related to androgen.

Results and conclusions

Two network pharmacology analyses indicated that Androgen receptor (AR) and fibroblast growth factor 2 (FGF2) are the candidate targets, suggesting that the mechanism of ED treatment by GLJC may be related to androgens and angiogenesis. Molecular docking further validated the effective binding of GLJC components to these two targets. In animal experiments, GLJC significantly increased the frequency of erections and elevated serum free testosterone levels and penile tissue AR expression in aged rats. GLJC also promoted angiogenesis and inhibited penile tissue fibrosis in aged rats by regulating the expression of FGF2, RICTOR/P-AKT/P-FOXO1. However, such regulation was not observed in orchiectomized rats. Therefore, GLJC increased testosterone utilization in d-galactose-induced aging rats and regulated FGF2, RICTOR/P-AKT/P-FOXO1 signaling pathway in a T-dependent manner, promoting corpus cavernosum survival and angiogenesis. This mechanism led to the inhibition of penile fibrosis.

背景及目的：贵灵鸡胶囊具有治疗勃起功能障碍（ED）的作用。本研究旨在探讨GLJC治疗ed的潜在机制。实验步骤：我们分别用TCMSP数据库中报道的GLJC成分和文献中报道的GLJC成分对ed相关靶点进行网络药理学分析。通过分子对接验证这些分子靶点的结合亲和力。动物实验验证了上述结果。以d-半乳糖诱导的衰老大鼠为实验对象研究GLJC治疗ED的机制，并以去睾丸大鼠为实验对象进一步探讨GLJC治疗ED的机制是否与雄激素有关。结果和结论两项网络药理学分析显示雄激素受体（AR）和成纤维细胞生长因子2 （FGF2）是候选靶点，提示GLJC治疗ED的机制可能与雄激素和血管生成有关。分子对接进一步验证了GLJC组分与这两个靶点的有效结合。在动物实验中，GLJC显著增加了老龄大鼠的勃起频率，提高了血清游离睾酮水平和阴茎组织AR表达。GLJC还通过调节FGF2、RICTOR/P-AKT/ p - fox01的表达，促进老年大鼠血管生成，抑制阴茎组织纤维化。然而，在切除睾丸的大鼠中没有观察到这种调节。因此，GLJC增加了d-半乳糖诱导衰老大鼠的睾酮利用，并以t依赖的方式调节FGF2、RICTOR/P-AKT/P-FOXO1信号通路，促进海肌体存活和血管生成。这一机制导致了阴茎纤维化的抑制。

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引用次数: 0

Traditional Chinese medicine as a protective strategy against chemotherapy-induced cardiotoxicity: An overview of the literature 中药作为化疗引起的心脏毒性的保护策略：文献综述

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-06-22 DOI: 10.1016/j.jtcme.2024.06.010

Jun-Wei Wang , Hong Shao , You-Ni Zhang , Tong Ge , Xiao-Yi Chen , Xiao-Zhou Mou

Cardiotoxicity refers to the damage caused to the heart or vascular system, which has become a significant cause of morbidity and mortality worldwide. Up to 20 % of adults undergoing cancer treatment may experience cardiotoxicity, with 7 %–10 % developing cardiomyopathy or heart failure. Cardiotoxic medications put patients at risk for a variety of heart conditions, including cardiac failure (HF), left ventricle (LV) systolic malfunction, cardiac arrhythmia, hypertension, coronary artery disease (CAD), and ischemia/myocardial infarction. These diseases may significantly impact the patient's quality of life and outcomes. Many conventional cancer chemotherapy agents have serious adverse effects. Anthracyclines, alkylating agents, taxanes, topoisomerase inhibitors, and antimetabolites are chemotherapeutic agents that induce cardiotoxicity. Recently, there has been an increasing focus on using traditional Chinese medicine (TCM) to treat chemotherapy-induced cardiotoxicity. TCM encompasses a range of practices, such as herbology, acupuncture, dietary therapy, and physical exercises like t'ai chi. These practices aim to enhance the flow of qi, which can alleviate symptoms of illness. Although the effectiveness of TCM has not been extensively researched and supported, scientists have begun utilizing scientific methods to gain a deeper understanding of the mechanisms underlying TCM. Ongoing research is being conducted to determine the safety and effectiveness of TCM treatments in reducing chemotherapy-induced toxicity. The present study aims to evaluate the protection and efficacy of various TCM treatments in chemotherapy-induced cardiotoxicity.

心脏毒性是指对心脏或血管系统造成的损害，它已成为世界范围内发病率和死亡率的重要原因。在接受癌症治疗的成年人中，高达20%的人可能会出现心脏毒性，7% - 10%的人会出现心肌病或心力衰竭。心脏毒性药物使患者面临各种心脏疾病的风险，包括心力衰竭（HF）、左心室（LV）收缩功能障碍、心律失常、高血压、冠状动脉疾病（CAD）和缺血/心肌梗死。这些疾病可能会严重影响患者的生活质量和预后。许多传统的癌症化疗药物都有严重的副作用。蒽环类药物、烷基化剂、紫杉烷、拓扑异构酶抑制剂和抗代谢物是诱导心脏毒性的化疗药物。近年来，人们越来越关注使用中药治疗化疗引起的心脏毒性。中医包括一系列的实践，如草药学、针灸、饮食疗法和像太极拳这样的体育锻炼。这些做法旨在加强气的流动，这可以减轻疾病的症状。虽然中药的有效性还没有得到广泛的研究和支持，但科学家们已经开始利用科学的方法来更深入地了解中药的潜在机制。目前正在进行研究，以确定中药治疗在减少化疗引起的毒性方面的安全性和有效性。本研究旨在评价各种中药治疗方法对化疗性心脏毒性的保护作用和疗效。

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引用次数: 0

Jieduquyuziyin prescription attenuates the side effect of prednisone through regulating gut microbiota when in the combination with prednisone treat MRL/lpr mice 洁尔阴处方与泼尼松联合治疗MRL/lpr小鼠时，通过调节肠道微生物群减轻泼尼松的副作用

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-05-24 DOI: 10.1016/j.jtcme.2024.05.005

Zhengyang Zhu , Mingzhu Wang , Lin Huang , Zhixing He

Jieduquyuziyin prescription (JP) is an empirical formula used to treat systemic lupus erythematosus (SLE). While JP has been shown to have synergistic and attenuated effects when combined with glucocorticoids (GCs) for SLE treatment, the precise mechanism remains unclear. This study utilized MRL/lpr mice to demonstrate the synergistic and attenuated effects of JP when combined with prednisone. Furthermore, a co-housing experiment was conducted to investigate whether JP-regulated gut microbiota had synergistic and attenuated effects in prednisone-treated MRL/lpr mice. The study found that JP exhibited synergistic effects only when combined with 5 mg/kg body weight prednisone, while its attenuated effects were observed with both 5 and 10 mg/kg body weight prednisone. Co-housing resulted in the transmission of gut microbiota between prednisone-treated and JP-treated MRL/lpr mice. However, co-housing did not enhance the therapeutic efficacy of prednisone; instead, it attenuated prednisone's adverse effects on liver inflammation (IL-6 and TNF-α) and serum cholesterol in MRL/lpr mice. The attenuated effects of JP may be associated with specific genera such as Akkermansia, Parasutterella, and Alistipes. These findings suggest that JP can mitigate the adverse effects of GCs by modulating gut microbiota during the treatment of SLE with GCs.

解毒祛瘀滋饮方是治疗系统性红斑狼疮（SLE）的经验方。虽然JP与糖皮质激素（GCs）联合治疗SLE具有协同和减弱作用，但确切的机制尚不清楚。本研究利用MRL/lpr小鼠来证明JP与强的松联合使用时的协同和减弱作用。此外，研究人员还进行了一项共舍实验，以研究jp调节的肠道微生物群在强的松治疗的MRL/lpr小鼠中是否具有协同和减毒作用。本研究发现，JP仅在与5mg /kg体重的强的松联合使用时才表现出协同作用，而在与5mg /kg体重的强的松联合使用时，JP均表现出减弱作用。共居导致泼尼松治疗和jp治疗的MRL/lpr小鼠之间肠道微生物群的传递。然而，共住房并没有提高强的松的治疗效果；相反，它减轻了强的松对MRL/lpr小鼠肝脏炎症（IL-6和TNF-α）和血清胆固醇的不良影响。JP的减弱效应可能与特定属有关，如Akkermansia， Parasutterella和Alistipes。这些研究结果表明，JP可以通过调节GCs治疗SLE期间的肠道微生物群来减轻GCs的不良反应。

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引用次数: 0

Potent anti-biofilm properties of plumbagin against fluconazole-resistant Candida auris plumbagin 对抗氟康唑念珠菌的强效抗生物膜特性

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-06-10 DOI: 10.1016/j.jtcme.2024.06.005

Hye-Won Jin , Yong-Bin Eom

Background and aim

The escalation of fungal infections is driving an increase in disease and mortality rates. In particular, the emergence of Candida auris (C. auris), which shows powerful resistance to the antifungal drug fluconazole, is becoming a global concern. Furthermore, several biological hurdles need to be overcome by candidate therapeutics because C. auris has the ability to form biofilm. Therefore, this study aimed to investigate the antifungal and anti-biofilm effects of plumbagin, a natural extract, against fluconazole-resistant C. auris (FRCA).

Experimental procedure

The minimum inhibitory concentrations (MICs) of fluconazole and plumbagin were determined against clinically isolated C. auris. Inhibition of biofilm formation and eradication effects of plumbagin against FRCA were confirmed through minimum biofilm inhibition concentration (MBIC) and minimum biofilm eradication concentration (MBEC) assays. Additionally, the inhibition of metabolic activity in biofilm cells was verified through quantification by XTT reduction assay and visualization by confocal laser scanning microscopy (CLSM). The relative expression levels of the azole resistant gene ERG11, the efflux pump gene CDR1, and the extracellular matrix gene KRE6, were measured.

Results and conclusion

Plumbagin exhibits antifungal efficacy against C. auris and has been shown to effectively inhibit both the formation and eradication of biofilms produced by FRCA. Furthermore, the metabolic activity inhibition in biofilm cells was both quantified and visually observed. The downregulation of all genes (ERG11, CDR1, and KRE6) by plumbagin was confirmed. Taken together, this study demonstrates that plumbagin has antifungal and anti-biofilm efficacy against FRCA, indicating its potential as an alternative to antifungal agents and a valuable resource in combating FRCA infections.

背景与目的真菌感染的升级正在推动疾病和死亡率的增加。特别是，对抗真菌药物氟康唑表现出强大耐药性的耳念珠菌（C. auris）的出现正成为全球关注的问题。此外，候选治疗方法需要克服几个生物学障碍，因为金黄色葡萄球菌具有形成生物膜的能力。因此，本研究旨在研究天然提取物白桦素对耐氟康唑金黄色葡萄球菌（FRCA）的抗真菌和抗生物膜作用。实验方法测定氟康唑和白丹素对临床分离的金黄色葡萄球菌的最低抑菌浓度（mic）。通过最小生物膜抑制浓度（MBIC）和最小生物膜根除浓度（MBEC）测定，证实了白桦素对FRCA的生物膜形成和根除作用。此外，通过XTT还原法定量和共聚焦激光扫描显微镜（CLSM）可视化验证了生物膜细胞代谢活性的抑制作用。测定抗唑基因ERG11、外排泵基因CDR1和细胞外基质基因KRE6的相对表达量。结果与结论白丹素对金黄色葡萄球菌具有一定的抗真菌作用，并能有效抑制FRCA生物膜的形成和清除。此外，对生物膜细胞的代谢活性抑制进行了定量和目视观察。证实白桦素下调了所有基因（ERG11、CDR1和KRE6）。综上所述，本研究表明白桦白素对FRCA具有抗真菌和抗生物膜的作用，表明其作为抗真菌药物的替代品和对抗FRCA感染的宝贵资源的潜力。

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引用次数: 0

Raddeanin A promotes the apoptosis of gastric cancer in conjunction with autophagy inhibitor Hydroxychloroquine via MAPK signaling pathway Raddeanin A 与自噬抑制剂羟氯喹通过 MAPK 信号通路共同促进胃癌细胞凋亡

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-07-20 DOI: 10.1016/j.jtcme.2024.07.004

Yuhao Teng , Ying Xing , Weiwei Xue , Yue Hu , Zirui Li , Jun Qian , Ruiping Wang

Purpose

Gastric cancer (GC) is among the malignant cancers with the highest incidence and mortality worldwide. As GC is not very sensitive to current chemotherapy drugs, there is an urgent need to develop new effective drugs. Raddeanin A (RA) is extracted from the traditional Chinese medicine Anemone raddeana Regel, which has an anti-cancer effect. The purpose of this study was to explore the effects of RA on GC in vitro and in vivo.

Methods

We explored the targets of RA in GC through network pharmacology. MTT assay, flow cytometry, Western blotting, and other methods were used to detect the effects of RA on the proliferation, apoptosis, and autophagy of GC cells. After preconditioning with hydroxychloroquine (HCQ) and rapamycin, we observed the effects of RA-induced autophagy on apoptosis. We further verified the antitumor effect and safety of RA in vivo. Using SNU-1 xenograft tumor model in nude mice, tumor volume was observed and liver toxicity was observed by immunohistochemistry.

Results

Many cancer-related signaling pathways were visualized using Cytoscape software. Among them, the MAPK signaling pathway was one of the highest-ranked pathways. The MTT assay results suggested that RA could inhibit the proliferation of HGC-27 and SNU-1 cells effectively. Flow cytometry and Western blotting confirmed that RA could significantly induce apoptosis of HGC-27 and SNU-1 cells. Electron microscopy and Western blotting demonstrated that RA could induce autophagy of HGC-27 and SNU-1 cells. Further experiments suggested that HCQ, an autophagy inhibitor, could enhance the capacity of RA to induce apoptosis. In animal studies, we found that intraperitoneal injection of RA could effectively and safely inhibit gastric tumors.

Conclusions

RA significantly inhibited the proliferation and induced autophagy and apoptosis of GC cells. In combination with HCQ, RA-induced apoptosis increased in vitro. The combined application of RA and autophagy inhibitors may serve as an added approach to the treatment of GC, but the underlying mechanism needs further exploration. In vivo, it was observed that RA has a good antitumor effect without increasing liver toxicity.

目的胃癌是世界上发病率和死亡率最高的恶性肿瘤之一。由于GC对现有化疗药物的敏感性不高，迫切需要开发新的有效药物。海葵素A （Raddeanin A， RA）是从中药海葵中提取的，具有抗癌作用。本研究的目的是探讨RA对体外和体内GC的影响。方法采用网络药理学方法，探索RA在GC中的作用靶点。采用MTT法、流式细胞术、Western blotting等方法检测RA对GC细胞增殖、凋亡和自噬的影响。在羟氯喹（HCQ）和雷帕霉素预处理后，观察ra诱导的自噬对细胞凋亡的影响。我们进一步在体内验证了RA的抗肿瘤作用和安全性。建立裸鼠移植瘤模型，采用免疫组化方法观察肿瘤体积和肝毒性。结果利用Cytoscape软件对多种肿瘤相关信号通路进行了可视化处理。其中，MAPK信号通路是排名最高的通路之一。MTT实验结果表明，RA能有效抑制HGC-27和SNU-1细胞的增殖。流式细胞术和Western blotting证实，RA能显著诱导HGC-27和SNU-1细胞凋亡。电镜和Western blot结果显示，RA可诱导HGC-27和SNU-1细胞自噬。进一步实验表明，自噬抑制剂HCQ可增强RA诱导细胞凋亡的能力。在动物实验中，我们发现腹腔注射RA能有效、安全地抑制胃肿瘤。结论ra能明显抑制胃癌细胞的增殖，诱导胃癌细胞自噬和凋亡。与HCQ联合，ra诱导的体外细胞凋亡增加。RA与自噬抑制剂联合应用可能是治疗胃癌的一种新途径，但其作用机制有待进一步探讨。在体内，观察到RA具有良好的抗肿瘤作用，且不增加肝毒性。

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引用次数: 0

Pediatric tuina treatment for spleen deficiency diarrhea regulated through the skin-brain-gut axis and mast cell degranulation 小儿推拿治疗脾虚泄泻的皮脑肠轴和肥大细胞脱颗粒调节作用

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-03-14 DOI: 10.1016/j.jtcme.2024.03.003

Yuetong Li , Shifang Fu , Fanyi Li , Yan Guo , Yanbo Cao , Fengjiao Ren , Rongrong Li , Yanguo Wang , Mingchi Luo

Background

Pediatric tuina is an effective alternative therapy for managing spleen deficiency diarrhea. The application of spleen-meridian and large-intestine-meridian points has been shown to alleviate symptoms and has garnered some support from evidence-based medicine. Nonetheless, there remains a dearth of research elucidating the biological effects of these specific acupoints. This study aimed to explore their effects by focusing on the material basis involving mast cells (MCs).

Methods

The experimental design induced spleen-deficiency diarrhea in Kunming mice through a 7-day administration of Rheum officinale extract through gavage. Following this induction, treatment was initiated, employing a combination of spleen-meridian and large-intestine-meridian points over 6 days. Efficacy was assessed using fecal scoring. Colonic structure was assessed through hematoxylin-eosin staining, while toluidine blue staining was employed to observe MC degranulation within the skin-brain-gut axis. Immunohistochemistry was performed to detect tryptase release from MCs.

Results

The treatment combining spleen-meridian and large-intestine-meridian points markedly ameliorated diarrhea symptoms and improved fecal scores in Kunming mice exhibiting spleen deficiency. Pediatric tuina treatment facilitated the restoration of the colonic barrier and reduction in MC counts within the skin acupoint-brain-gut axis, consequently affecting the biologically active substance tryptase.

Conclusion

This study reveals the biological mechanism underlying the efficacy of specific acupoints in pediatric tuina, employing a holistic perspective encompassing the skin-brain-gut axis and MCs. Our findings substantiate the scientific basis for the effectiveness of tuina therapy in managing diarrhea and offer a new avenue for fundamental research on specific acupoints within pediatric tuina.

背景小儿推拿是治疗脾虚腹泻的有效替代疗法。脾经和大肠经穴位的应用已被证明可以缓解症状，并得到了一些循证医学的支持。尽管如此，仍然缺乏研究阐明这些特定穴位的生物学效应。本研究旨在从涉及肥大细胞（MCs）的物质基础上探讨其作用。方法采用大黄提取物灌胃诱导昆明小鼠脾虚腹泻7 d的实验设计。诱导后，开始脾经和大肠经联合治疗，持续6天。采用粪便评分法评估疗效。苏木精-伊红染色评估结肠结构，甲苯胺蓝染色观察皮肤-脑-肠轴MC脱粒。免疫组化检测MCs中胰蛋白酶的释放。结果脾经与大肠经结合治疗能明显改善脾虚小鼠腹泻症状，改善粪便评分。小儿推拿治疗促进了结肠屏障的恢复和皮肤腧穴-脑-肠轴内MC计数的减少，从而影响了生物活性物质胰蛋白酶。结论本研究从皮肤-脑-肠轴和MCs的整体角度揭示了小儿推拿特定穴位疗效的生物学机制。本研究结果为推拿治疗腹泻的有效性提供了科学依据，并为小儿推拿特定穴位的基础研究提供了新的途径。

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引用次数: 0

Withdrawal notice to: “Knowledge and attitudes towards utilizing complementary and alternative medical (CAM) treatments by mental health practitioner from various disciplines” [J Tradit Complement Med 13 (6) (2023) 640] 撤回通知：“各学科心理健康从业者对利用补充和替代医学（CAM）治疗的知识和态度” [J Tradit complementary Med 13 (6) (2023) 640]

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-12-19 DOI: 10.1016/j.jtcme.2024.12.002

Sharon Freeman Clevenger

引用次数: 0

Study on the pharmacodynamics and related mechanism of Tangningtongluo tablet on prediabetes mice based on the theory of “liver controlling dispersion” 基于“控肝散”理论的糖宁通络片对糖尿病前期小鼠的药效学及相关机制研究

IF 3.3 3区医学 Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE

Journal of Traditional and Complementary Medicine

Pub Date : 2025-03-01 Epub Date: 2024-06-28 DOI: 10.1016/j.jtcme.2024.06.011

Xiangka Hu , Liuming Gui , Mushuang Qi , Wanjun Zhu , Ying Ren , Jin Li , Shuyu Yang , Chunmei Dai

Background and aim

Prediabetes is an unavoidable process and a high risk factor for developing of type 2 diabetes. Tangningtongluo (TNTL) tablet is a kind of pure plant preparation in hospital and used for the diabetes (消渴病, xiāo kě bìng) caused by deficiency of both Qi and Yin (气阴两虚，qì yīn liǎng xū). However, the effect of TNTL tablet on prediabetes has not been reported for now. This study was aimed to investigate the effect and related mechanism of TNTL tablet on prediabetes.

Experimental procedure

Prediabetic mice induced by a high-sugar and high-fat diet combined with streptozotocin were treated with TNTL tablet, and the pharmacodynamics and related mechanism were studied.

Results and conclusion

Our results showed that TNTL tablet reduced body weight and regulated the disorder of glucose and lipid metabolism in prediabetic mice. The function and the pathological changes of liver and islet tissue were improved after TNTL tablet treated prediabetic mice. Additionally, TNTL tablet decreased the levels of MDA, TNF-α, IL-1β and IL-6 in serum, increased the contents of SOD and GSH-px, up-regulated the expression of p-PI3K and p-AKT protein, and down-regulated the expression of p-IKK and p-NF-κB p65 protein in liver tissue. This study revealed that TNTL tablet could improve insulin sensitivity and insulin resistance in prediabetic mice, and delay the procession of prediabetes to diabetes, which might be related to inhibiting IKK/NF-κB signaling pathway, exerting anti-inflammatory and antioxidant effects, and activating PI3K/AKT signaling pathway.

背景与目的糖尿病前期是2型糖尿病不可避免的发病过程，是发生2型糖尿病的高危因素。糖宁通络片（TNTL）是一种医院用纯植物制剂，用于治疗气阴两虚（,qì n liǎng）引起的糖尿病（）。然而，TNTL片对前驱糖尿病的影响目前尚未见报道。本研究旨在探讨TNTL片对糖尿病前期的影响及其作用机制。实验步骤采用TNTL片治疗高糖高脂饮食联合链脲佐菌素诱导的糖尿病前期小鼠，研究其药效学及作用机制。结果与结论TNTL片对糖尿病前期小鼠具有减轻体重和调节糖脂代谢紊乱的作用。TNTL片对糖尿病前期小鼠的肝脏和胰岛组织功能及病理改变均有改善作用。此外，TNTL片降低血清MDA、TNF-α、IL-1β、IL-6水平，升高SOD、GSH-px含量，上调肝组织中p-PI3K、p-AKT蛋白表达，下调p-IKK、p-NF-κB p65蛋白表达。本研究发现，TNTL片可改善糖尿病前期小鼠胰岛素敏感性和胰岛素抵抗，延缓糖尿病前期向糖尿病的发展，其作用机制可能与抑制IKK/NF-κB信号通路，发挥抗炎、抗氧化作用，激活PI3K/AKT信号通路有关。

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