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Chinese Materia Medica in Treating Depression: The Role of Intestinal Microenvironment. 中药治疗抑郁症:肠道微环境的作用。
Pub Date : 2023-01-01 Epub Date: 2023-11-04 DOI: 10.1142/S0192415X23500854
Ruhui Shen, Zhipeng Li, Huiyun Wang, Yongchao Wang, Xiaofang Li, Qian Yang, Yingjie Fu, Ming Li, Li-Na Gao

Depression is a highly heterogeneous mental illness. Drug treatment is currently the main therapeutic strategy used in the clinic, but its efficacy is limited by the modulation of a single target, slow onset, and side effects. The gut-brain axis is of increasing interest because intestinal microenvironment disorders increase susceptibility to depression. In turn, depression affects intestinal microenvironment homeostasis by altering intestinal tissue structure, flora abundance and metabolism, hormone secretion, neurotransmitter transmission, and immune balance. Depression falls into the category of "stagnation syndrome" according to Traditional Chinese Medicine (TCM), which further specifies that "the heart governs the spirit and is exterior-interior with the small intestine". However, the exact mechanisms of the means by which the disordered intestinal microenvironment affects depression are still unclear. Here, we present an overview of how the Chinese materia medica (CMM) protects against depression by repairing intestinal microenvironment homeostasis. We review the past five years of research progress in classical antidepressant TCM formulae and single CMMs on regulating the intestinal microenvironment for the treatment of depression. We then analyze and clarify the multitarget functions of CMM in repairing intestinal homeostasis and aim to provide a new theoretical basis for CMM clinical application in the treatment of depression.

抑郁症是一种高度异质性的精神疾病。药物治疗是目前临床上使用的主要治疗策略,但其疗效受到单一靶点调节、起效缓慢和副作用的限制。肠脑轴越来越受到关注,因为肠道微环境紊乱增加了抑郁症的易感性。反过来,抑郁症通过改变肠道组织结构、菌群丰度和代谢、激素分泌、神经递质传递和免疫平衡来影响肠道微环境稳态。抑郁症在中医学上属于“郁证”范畴,进一步明确了“心主神,以小肠为表内”。然而,紊乱的肠道微环境影响抑郁症的确切机制尚不清楚。在这里,我们概述了中药如何通过修复肠道微环境稳态来预防抑郁症。我们回顾了过去五年来经典抗抑郁中药配方和单一CMMs在调节肠道微环境治疗抑郁症方面的研究进展。然后,我们分析和阐明了CMM在修复肠道稳态中的多靶点功能,旨在为CMM在抑郁症治疗中的临床应用提供新的理论依据。
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引用次数: 0
Research Progress and New Perspectives of Anticancer Effects of Emodin. 大黄素抗癌作用研究进展及新进展。
Pub Date : 2023-01-01 Epub Date: 2023-09-21 DOI: 10.1142/S0192415X23500787
Wu Liu, Eskandar Qaed, Yuelin Zhu, Wenzhang Tian, Yizhen Wang, Le Kang, Xiaodong Ma, Zeyao Tang

Emodin is a natural compound found in several traditional Chinese medicines, including Rheum palmatum and Polygonum cuspidatum. Recent studies have shown that emodin exhibits potent anticancer effects against a variety of cancer types, including liver, breast, lung, and colon cancer. Emodin's anticancer effects are mediated through several mechanisms, including inhibition of cell proliferation, induction of apoptosis, and suppression of tumor angiogenesis and metastasis. In this review, we provide an overview of recent research progress and new perspectives on emodin's anticancer effect. We summarize the current understanding of the molecular mechanisms underlying emodin's anticancer activity, including its effects on signaling pathways such as the PI3K/Akt, MAPK, and NF-[Formula: see text]B pathways. We also discuss the potential of emodin as a therapeutic agent for cancer treatment, including its use in combination with conventional chemotherapeutic drugs and as a sensitizer for radiotherapy. Furthermore, we highlight recent advances in the development of emodin derivatives and their potential as novel anticancer agents. Finally, we discuss the challenges and opportunities for the translation of emodin's anticancer properties into clinical applications, including the need for further preclinical and clinical studies to evaluate its safety and efficacy. In conclusion, emodin represents a promising natural compound with potent anticancer properties, and its potential as a therapeutic agent for cancer treatment warrants further investigation. This review provides a comprehensive overview of the current research progress and new perspectives on emodin's anticancer effects, which may facilitate the development of novel therapeutic strategies for cancer treatment.

大黄素是一种天然化合物,存在于几种中药中,包括大黄和虎杖。最近的研究表明,大黄素对多种癌症类型表现出强大的抗癌作用,包括肝癌、乳腺癌、肺癌和癌症。大黄素的抗癌作用是通过几种机制介导的,包括抑制细胞增殖、诱导细胞凋亡以及抑制肿瘤血管生成和转移。在这篇综述中,我们概述了大黄素抗癌作用的最新研究进展和新的前景。我们总结了目前对大黄素抗癌活性的分子机制的理解,包括其对PI3K/Akt、MAPK和NF-[公式:见正文]B通路等信号通路的影响。我们还讨论了大黄素作为癌症治疗剂的潜力,包括其与传统化疗药物联合使用以及作为放射治疗的增敏剂。此外,我们还重点介绍了大黄素衍生物的开发进展及其作为新型抗癌剂的潜力。最后,我们讨论了将大黄素的抗癌特性转化为临床应用的挑战和机遇,包括需要进一步的临床前和临床研究来评估其安全性和有效性。总之,大黄素是一种具有强大抗癌特性的有前景的天然化合物,其作为癌症治疗剂的潜力值得进一步研究。这篇综述对大黄素抗癌作用的研究进展和新观点进行了全面综述,可能有助于开发新的癌症治疗策略。
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引用次数: 0
Andrographolide Attenuates Oxidized LDL-Induced Activation of the NLRP3 Inflammasome in Bone Marrow-Derived Macrophages and Mitigates HFCCD-Induced Atherosclerosis in Mice. 穿心莲内酯减轻氧化低密度脂蛋白诱导的骨髓来源巨噬细胞中NLRP3炎症小体的激活,并减轻HFCCD诱导的小鼠动脉粥样硬化。
Pub Date : 2023-01-01 Epub Date: 2023-11-04 DOI: 10.1142/S0192415X23500933
Chih-Chieh Chen, Chong-Kuei Lii, Kai-Li Liu, Yi-Ling Lin, Chia-Wen Lo, Chien-Chun Li, Ya-Chen Yang, Haw-Wen Chen

Andrographolide (AND) is a bioactive component of the herb Andrographis paniculata and a well-known anti-inflammatory agent. Atherosclerosis is a chronic inflammatory disease of the vasculature, and oxidized LDL (oxLDL) is thought to contribute heavily to atherosclerosis-associated inflammation. The aim of this study was to investigate whether AND mitigates oxLDL-mediated foam cell formation and diet-induced atherosclerosis (in mice fed a high-fat, high-cholesterol, high-cholic acid [HFCCD] diet) and the underlying mechanisms involved. AND attenuated LPS/oxLDL-mediated foam cell formation, IL-1[Formula: see text] mRNA and protein (p37) expression, NLR family pyrin domain containing 3 (NLRP3) mRNA and protein expression, caspase-1 (p20) protein expression, and IL-1[Formula: see text] release in BMDMs. Treatment with oxLDL significantly induced protein and mRNA expression of CD36, lectin-like oxLDL receptor-1 (LOX-1), and scavenger receptor type A (SR-A), whereas pretreatment with AND significantly inhibited protein and mRNA expression of SR-A only. Treatment with oxLDL significantly induced ROS generation and Dil-oxLDL uptake; however, pretreatment with AND alleviated oxLDL-induced ROS generation and Dil-oxLDL uptake. HFCCD feeding significantly increased aortic lipid accumulation, ICAM-1 expression, and IL-1[Formula: see text] mRNA expression, as well as blood levels of glutamic pyruvic transaminase (GPT), total cholesterol, and LDL-C. AND co-administration mitigated aortic lipid accumulation, the protein expression of ICAM-1, mRNA expression of IL-1[Formula: see text] and ICAM-1, and blood levels of GPT. These results suggest that the working mechanisms by which AND mitigates atherosclerosis involve the inhibition of foam cell formation and NLRP3 inflammasome-dependent vascular inflammation as evidenced by decreased SR-A expression and IL-1[Formula: see text] release, respectively.

穿心莲内酯(AND)是穿心莲的一种生物活性成分,也是一种著名的抗炎药。动脉粥样硬化是一种血管系统的慢性炎症性疾病,氧化低密度脂蛋白(oxLDL)被认为是动脉粥样硬化相关炎症的主要原因。本研究的目的是研究AND是否减轻oxLDL介导的泡沫细胞形成和饮食诱导的动脉粥样硬化(在喂食高脂肪、高胆固醇、高胆酸[HFCD]饮食的小鼠中)以及相关的潜在机制。AND减弱了LPS/oxLDL介导的泡沫细胞形成、IL-1【公式:见正文】mRNA和蛋白(p37)表达、NLR家族pyrin结构域包含3(NLRP3)mRNA和蛋白表达、胱天蛋白酶1(p20)蛋白表达和IL-1【配方:见正文)在BMDMs中的释放。oxLDL处理显著诱导CD36、凝集素样oxLDL受体-1(LOX-1)和清除剂受体A型(SR-A)的蛋白质和mRNA表达,而and预处理仅显著抑制SR-A的蛋白质和信使表达。oxLDL处理显著诱导ROS的产生和Dil-oxLDL的摄取;然而,用AND预处理减轻了oxLDL诱导的ROS的产生和Dil-oxLDL的摄取。HFCCD喂养显著增加了主动脉脂质积聚、ICAM-1表达和IL-1[公式:见正文]mRNA表达,以及血液中谷丙转氨酶(GPT)、总胆固醇和LDL-C的水平。AND联合给药减轻了主动脉脂质积聚、ICAM-1的蛋白表达、IL-1的mRNA表达[公式:见正文]和ICAM-1,以及GPT的血液水平。这些结果表明,AND缓解动脉粥样硬化的工作机制包括抑制泡沫细胞形成和NLRP3炎症小体依赖性血管炎症,分别通过降低SR-A表达和IL-1释放来证明。
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引用次数: 0
Triterpenoid Compounds from Cyclocarya paliurus: A Review of Their Phytochemistry, Quality Control, Pharmacology, and Structure-Activity Relationship. 黄柏三萜类化合物:植物化学、质量控制、药理及构效关系研究进展
Pub Date : 2023-01-01 Epub Date: 2023-11-10 DOI: 10.1142/S0192415X2350088X
Shuran Zhang, Junyu He, Jie Li, Haibo He, Yumin He, Xiao Wang, Heng Shu, Jihong Zhang, Daoxiang Xu, Kun Zou

Cyclocarya paliurus (Batalin) Iljinskaja (C. paliurus) is a single species of Cyclocarya paliurus in Juglandaceae. It is a unique rare medicinal plant resource in China that is mainly distributed in the south of China. The leaves of C. paliurus, as a new food ingredient, are processed into tea products in daily life. Triterpenoids are the main active ingredient in C. paliurus. So far, 164 triterpenoid compounds have been isolated and identified from C. paliurus, which are included 3,4-seco-dammaranes, dammaranes, oleanane, ursane, lupinanes, taraxeranes, and norceanothanes. Modern pharmacological studies manifested that these ingredients have a wide range of pharmacological activities both in vitro and in vivo, such as reducing blood sugar, lowering blood lipids, and anti-tumor, anti-inflammatory, anti-oxidant, and other activities. In addition, current results indicate that the pharmacological mechanisms of triterpenoids were closely related to their chemical structure, molecular signaling pathways, and the expression of related proteins. In order to further study C. paliurus based on the current research situation, this review summarizes the prospect and systematic summary of the triterpenes of C. paliurus from the aspects of structural characteristics, quality control, biological activity, and the structure-activity relationship, which provide a reference for further research and application of the triterpenoids from C. paliurus in the field of functional food and medicine.

巴柳青是核桃科巴柳青属植物的一种。它是中国独特的稀有药用植物资源,主要分布在中国南方。枸杞叶作为一种新型的食品原料,在日常生活中被加工成茶叶制品。三萜类化合物是凤尾草的主要有效成分。到目前为止,已从枸杞中分离鉴定出了164个三萜化合物,包括3,4-仲达玛烷、达玛烷、齐墩烷、熊烷、羽扇豆烷、taraxer烷和去鲸烷。现代药理学研究表明,这些成分具有广泛的体内外药理活性,如降血糖、降血脂,以及抗肿瘤、抗炎、抗氧化等活性。此外,目前的研究结果表明,三萜的药理机制与其化学结构、分子信号通路以及相关蛋白的表达密切相关。为了在现有研究现状的基础上进一步研究苍蝇子,本文从结构特征、质量控制、生物活性、构效关系等方面对苍蝇子三萜的研究前景进行了综述和系统总结,为苍蝇子三萜在功能食品和医药领域的进一步研究和应用提供参考。
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引用次数: 0
Ginsenoside Rd Inhibited Ferroptosis to Alleviate CCl4-Induced Acute Liver Injury in Mice via cGAS/STING Pathway. 人参皂苷Rd通过cGAS/STING途径抑制铁中毒减轻ccl4诱导的小鼠急性肝损伤
Pub Date : 2022-11-28 DOI: 10.2139/ssrn.4100254
Yuangeng Li, Ping Yu, Wenwen Fu, Shuo Wang, Wenjun Zhao, Yue Ma, Yi Wu, Heming Cui, Xiaofeng Yu, L. Fu, Huali Xu, Dayun Sui
Carbon tetrachloride (CCl4)-induced lipid peroxidation associated with hepatic oxidative stress and cell death is an important mechanism of acute liver injury (ALI). Ginsenoside Rd is considered an active ingredient of ginseng. Evidence suggests that ginsenoside Rd may improve ischaemic stroke, nerve damage, cancer and other diseases involving apoptosis, inflammation, oxidative stress, mitochondrial injury and autophagy. However, the effects of ginsenoside Rd on CCl4-induced ALI and its underlying mechanisms are still unclear. In this study, 0.25% CCl4 was injected intraperitoneally in mice to establish a CCl4-induced ALI model. In the Rd treatment group, Rd (10, 20[Formula: see text]mg/kg) doses were injected intraperitoneally 1[Formula: see text]h before and 23[Formula: see text]h after CCl4 administration. Ferroptosis inducer imidazole ketone erastin (IKE) was injected intraperitoneally 4[Formula: see text]h before CCl4 administration to explore the mechanism. The blood and liver were collected 24[Formula: see text]h after CCl4 administration to investigate the effect and mechanism of ginsenoside Rd on CCl4-induced ALI. Our results showed that ginsenoside Rd inhibited CCl4-induced ALI in mice. Ginsenoside Rd also downregulated CCl4-induced serum and liver iron, 4-hydroxynonenal, and 8-hydroxy-2 deoxyguanosine levels. Furthermore, it upregulated glutathione and glutathione peroxidase 4 levels. In addition, ginsenoside Rd downregulated the expression of cGAS and STING. Subsequently, the ferroptosis inducer imidazole ketone erastin significantly reversed the hepatoprotective effect and influence of ginsenoside Rd with regard to the indicators mentioned above. Our study confirmed that ginsenoside Rd ameliorated CCl4-induced ALI in mice, which was related to the reduction of ferroptosis. Simultaneously, the ginsenoside Rd-mediated inhibition of the cGAS/STING pathway contributed to its antiferroptosis effect. In conclusion, our results suggested that ginsenoside Rd inhibited ferroptosis via the cGAS/STING pathway, thereby protecting mice from CCl4-induced ALI. These results suggested ginsenoside Rd may be used as a potential intervention treatment against CCl4-induced ALI.
四氯化碳(CCl4)诱导的脂质过氧化与肝脏氧化应激和细胞死亡相关,是急性肝损伤(ALI)的重要机制。人参皂苷Rd被认为是人参的一种活性成分。有证据表明,人参皂苷Rd可能改善缺血性中风、神经损伤、癌症和其他涉及细胞凋亡、炎症、氧化应激、线粒体损伤和自噬的疾病。然而,人参皂苷Rd对ccl4诱导的ALI的作用及其机制尚不清楚。本研究通过腹腔注射0.25% CCl4,建立CCl4诱导的小鼠ALI模型。Rd组在CCl4给药前1 h,给药后23 h,分别腹腔注射Rd(10、20 mg/kg)剂量。在CCl4给药前腹腔注射铁下垂诱导剂咪唑酮erastin (imidazole酮erastin, IKE)[公式:见文],探讨其作用机制。给药24 h后取血、取肝,探讨人参皂苷Rd对CCl4诱导ALI的作用及机制。结果表明,人参皂苷Rd对ccl4诱导的小鼠ALI有抑制作用。人参皂苷Rd也下调ccl4诱导的血清和肝脏铁、4-羟基壬烯醛和8-羟基-2脱氧鸟苷水平。此外,它还上调谷胱甘肽和谷胱甘肽过氧化物酶4的水平。此外,人参皂苷Rd下调cGAS和STING的表达。随后,铁下垂诱导剂咪唑酮erastin在上述指标上显著逆转了人参皂苷Rd的肝保护作用和影响。我们的研究证实,人参皂苷Rd可以改善ccl4诱导的小鼠ALI,这与降低铁下垂有关。同时,人参皂苷rd介导的对cGAS/STING通路的抑制有助于其抗铁下垂作用。总之,我们的研究结果表明,人参皂苷Rd通过cGAS/STING途径抑制铁凋亡,从而保护小鼠免受ccl4诱导的ALI。这些结果提示人参皂苷Rd可能作为ccl4诱导的ALI的潜在干预治疗。
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引用次数: 9
Amygdalin Induced Mitochondria-Mediated Apoptosis of Lung Cancer Cells via Regulating NF[Formula: see text]B-1/NF[Formula: see text]B Signaling Cascade in Vitro and in Vivo. 苦杏仁苷诱导线粒体介导的肺癌症细胞凋亡通过调节NF-公式:见正文]B-1/NF[公式:见文本]B信号级联在体外和体内。
Pub Date : 2022-06-08 DOI: 10.1142/S0192415X22500586
Shumeng Lin, Jing Wen, Xiao Xu, Jiamin Shi, Wen Zhang, Tiansheng Zheng, Yaqin Hou, Yanfei Zhang, Zi-wei Li, Kai Wang, Jing Jin, Liduo Yue, Baigenzhin Abay, Ming Li, Qingxi Yue, L. Fan
Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer death worldwide. Amygdalin, a natural compound commonly distributed in plants of the Rosaceae species, owns anticancer activity, less side effects, wide source, and relatively low price. Although the apoptosis is a central process activated by amygdalin in cancer cells, the underlying molecular mechanisms through which amygdalin induces the apoptosis of lung cancer cells remain poorly understood. In this research work, amygdalin could suppress the proliferation of lung cancer A549 and PC9 cells by CCK8 assay. Amygdalin significantly promoted the apoptosis of lung cancer A549 and PC9 cells stained with Annexin V-FITC/PI by flow cytometry assay. Furthermore, amygdalin dose-dependently decreased the mitochondrial membrane potential (MMP) with JC-1 dye by flow cytometry. To investigate the underlying molecular mechanisms through which amygdalin induced mitochondria-mediated apoptosis of cancer cells, the differentially-expressed genes with a fold change >2.0 and [Formula: see text] < 0.05 were acquired from the cDNA microarray analysis. The results of qRT-PCR further confirmed that the differentially-expressed level of the NF[Formula: see text]B-1 gene was most obviously enhanced in lung cancer cells treated with amygdalin. The results of immunofluorescence staining, Western blotting and siRNA knockdown indicated that amygdalin induced mitochondria-mediated apoptosis of lung cancer cells via enhancing the expression of NF[Formula: see text]B-1 and inactivating NF[Formula: see text]B signaling cascade and further changing the expressions of proteins (Bax, Bcl-2, cytochrome C, caspase 9, caspase 3 and PARP) related to apoptosis, which were further checked by in vivo study of the lung cancer cell xenograft mice model accompanying with immunohistochemical staining and TUNEL staining. Our results indicated that amygdalin might be a potential activator of NF[Formula: see text]B-1, which sheds more light on the molecular mechanism of anticancer effects of amygdalin. These results highlighted amygdalin as a potential therapeutic anticancer agent, which warrants its development as a therapy for lung cancer.
肺癌是世界上最常见的癌症,也是癌症死亡的主要原因。苦杏仁苷是一种普遍存在于蔷薇科植物中的天然化合物,具有抗癌活性强、副作用小、来源广泛、价格较低等优点。虽然细胞凋亡是由苦杏仁苷激活的中心过程,但苦杏仁苷诱导肺癌细胞凋亡的潜在分子机制尚不清楚。本研究通过CCK8实验发现,苦杏仁苷能抑制肺癌A549和PC9细胞的增殖。流式细胞术检测苦杏仁苷对Annexin V-FITC/PI染色的肺癌A549和PC9细胞凋亡有显著促进作用。此外,流式细胞术显示苦杏仁苷剂量依赖性地降低了JC-1染色的线粒体膜电位(MMP)。为了研究苦杏仁苷诱导线粒体介导的癌细胞凋亡的潜在分子机制,我们通过cDNA芯片分析获得了突变倍数>2.0和[公式:见文]< 0.05的差异表达基因。qRT-PCR结果进一步证实,NF[公式:见文]B-1基因的差异表达水平在苦杏仁苷处理的肺癌细胞中增强最为明显。免疫荧光染色、Western blotting和siRNA敲除结果显示,苦杏仁苷通过增强NF[公式:见文]B-1的表达和使NF[公式:]失活来诱导线粒体介导的肺癌细胞凋亡。B信号级联并进一步改变与凋亡相关的蛋白(Bax、Bcl-2、细胞色素C、caspase 9、caspase 3和PARP)的表达,通过免疫组化染色和TUNEL染色的肺癌细胞异种移植小鼠模型的体内研究进一步验证。我们的研究结果表明,苦杏仁苷可能是NF的潜在激活剂[公式:见文]B-1,这进一步揭示了苦杏仁苷抗癌作用的分子机制。这些结果突出了苦杏仁苷作为一种潜在的抗癌治疗药物,值得其作为肺癌治疗的发展。
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引用次数: 3
Sinomenium acutum: A Comprehensive Review of its Botany, Phytochemistry, Pharmacology and Clinical Application. 尖青藤:植物学、植物化学、药理学和临床应用综述。
Pub Date : 2022-06-08 DOI: 10.1142/S0192415X22500501
Chao Ding, Yu-ze Li, Yu Sun, Ying Wu, Fengrui Wang, Chenwang Liu, Huawei Zhang, Yi Jiang, Dongdong Zhang, Xiaomei Song
Sinomenium acutumis the dry stem of Sinomenium acutum (Thunb.) Rehd et Wils. (S. acutum) and Sinomenium acutum(Thunb.) Rehd. et Wils. var. cinereumRehd. et Wils and is mainly distributed in China and Japan. As a traditional Chinese medicine (TCM) for dispelling wind and dampness in China, it is widely distributed and has a long history of drug use. In recent years, with the increase of the incidence of rheumatoid disease, S. acutum has become the focus of research. This paper reviews the literature on the chemical constituents, pharmacological effects, clinical applications and pharmacokinetics and safety of S. acutum from the past 60 years. At present, more than 210 natural compounds have been isolated from S. acutum, including alkaloids, lignans, triterpenoid saponins, steroids, and other structures. Pharmacological activities of S. acutum were mainly reported on anti-inflammatory, analgesic, anti-allergic, immunosuppressive, anti-tumor, liver-protective, anti-oxidative, and other effects, and clinical applications were mainly recorded on rheumatoid arthritis, ankylosing spondylitis, and other diseases. The clinical use of SIN has fewer side effects and more safety; only a small number of gastrointestinal reactions occurred, and the symptoms disappeared after the drug stopped. The purpose of this paper is to lay a foundation and provide reference for the follow-up research and wide application of S. acutum.
尖青藤是尖青藤的干燥茎。(S.acutum)和青藤(Sinomenium acutum(Thunb.)Rehd。et Wils。变种cinereumRehd。et Wils,主要分布于中国和日本。作为一种祛风除湿的中药,在我国分布广泛,用药历史悠久。近年来,随着类风湿性关节炎发病率的增加,尖尖孢菌成为研究的热点。本文综述了近60年来关于麻风子的化学成分、药理作用、临床应用及药代动力学和安全性的文献。目前,已从尖尖孢中分离出210多种天然化合物,包括生物碱、木脂素、三萜皂苷、甾体等结构。尖锐湿疣的药理活性主要有抗炎、镇痛、抗过敏、免疫抑制、抗肿瘤、护肝、抗氧化等作用,临床应用主要有类风湿性关节炎、强直性脊柱炎等疾病的记载。SIN的临床应用具有较少的副作用和更高的安全性;只有少量胃肠道反应发生,停药后症状消失。本文旨在为麻风子的后续研究和广泛应用奠定基础和提供参考。
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引用次数: 4
Lupeol Alleviates Myocardial Ischemia-Reperfusion Injury in Rats by Regulating NF-[Formula: see text]B and Nrf2 Pathways. 狼疮通过调节NF-(公式:见正文)B和Nrf2通路减轻大鼠心肌缺血再灌注损伤。
Pub Date : 2022-06-04 DOI: 10.1142/S0192415X22500525
Jing Li, Xuming Ma, Jun Yang, Lu Wang, Yan Huang, Yan Zhu
Cardiovascular disease is a global health problem. Previous studies revealed that it involves acute myocardial infarction and ischemia-reperfusion (I/R) injury. The mechanism of myocardial I/R injury is complex. But recognizing its mechanisms will bring important clinical significance. Lupeol is widely found in Chinese medicinal herbs and has been shown to have a variety of bio-activities. However, the pharmacological action of lupeol in the progress of myocardial ischemia-reperfusion injury (MIRI) is unclear. This study used a rat myocardial I/R model and the morphological changes in myocardium were determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The expression levels of IL-10, IL-1[Formula: see text], TNF-[Formula: see text], and IL-6 were assessed by quantitative real-time PCR (qRT-PCR) and ELISA. The expression levels of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) level and inflammatory cytokines were quantified using ELISA. The cellular apoptotic rate was determined by TUNEL staining. The findings showed that lupeol significantly decreased myocardial infarction after I/R and ameliorated I/R-induced myocardial inflammation, apoptosis, and oxidative stress. Furthermore, our results suggested that lupeol protected against MIRI-induced myocardial infarction through modulation of NF-[Formula: see text]B and Nrf2 signaling pathways. In summary, this study first clarified the cardioprotective effects of lupeol against I/R-induced myocardial infarction in rats, which could be due to its anti-oxidant, anti-inflammatory, and anti-apoptotic activities. Our study also highlighted a mechanism of NF-[Formula: see text]B and Nrf2 signaling, through which lupeol could be a promising agent in protecting against I/R-induced myocardial infarction.
心血管疾病是一个全球性的健康问题。先前的研究表明,它涉及急性心肌梗死和缺血再灌注(I/R)损伤。心肌I/R损伤机制复杂。但认识其机制将带来重要的临床意义。木犀草素广泛存在于中草药中,并已被证明具有多种生物活性。然而,羽扇豆醇在心肌缺血再灌注损伤(MIRI)过程中的药理作用尚不清楚。本研究采用大鼠心肌I/R模型,用2,3,5-三苯基氯化四氮唑(TTC)染色法测定心肌的形态学变化。通过实时定量PCR(qRT-PCR)和ELISA评估IL-10、IL-1[公式:见正文]、TNF-[公式:见正文]和IL-6的表达水平。酶联免疫吸附法测定肌酸激酶MB同工酶(CK-MB)、乳酸脱氢酶(LDH)和炎性细胞因子的表达水平。TUNEL染色测定细胞凋亡率。研究结果表明,羽扇豆醇显著减少I/R后的心肌梗死,并改善I/R诱导的心肌炎症、细胞凋亡和氧化应激。此外,我们的研究结果表明,羽扇豆醇通过调节NF-[公式:见正文]B和Nrf2信号通路,对MIRI诱导的心肌梗死具有保护作用。总之,本研究首次阐明了羽扇豆醇对I/R诱导的大鼠心肌梗死的心脏保护作用,这可能是由于其抗氧化、抗炎和抗凋亡活性。我们的研究还强调了NF-[公式:见正文]B和Nrf2信号传导的机制,通过该机制,羽扇豆醇可能是一种很有前途的预防I/R诱导的心肌梗死的药物。
{"title":"Lupeol Alleviates Myocardial Ischemia-Reperfusion Injury in Rats by Regulating NF-[Formula: see text]B and Nrf2 Pathways.","authors":"Jing Li, Xuming Ma, Jun Yang, Lu Wang, Yan Huang, Yan Zhu","doi":"10.1142/S0192415X22500525","DOIUrl":"https://doi.org/10.1142/S0192415X22500525","url":null,"abstract":"Cardiovascular disease is a global health problem. Previous studies revealed that it involves acute myocardial infarction and ischemia-reperfusion (I/R) injury. The mechanism of myocardial I/R injury is complex. But recognizing its mechanisms will bring important clinical significance. Lupeol is widely found in Chinese medicinal herbs and has been shown to have a variety of bio-activities. However, the pharmacological action of lupeol in the progress of myocardial ischemia-reperfusion injury (MIRI) is unclear. This study used a rat myocardial I/R model and the morphological changes in myocardium were determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The expression levels of IL-10, IL-1[Formula: see text], TNF-[Formula: see text], and IL-6 were assessed by quantitative real-time PCR (qRT-PCR) and ELISA. The expression levels of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) level and inflammatory cytokines were quantified using ELISA. The cellular apoptotic rate was determined by TUNEL staining. The findings showed that lupeol significantly decreased myocardial infarction after I/R and ameliorated I/R-induced myocardial inflammation, apoptosis, and oxidative stress. Furthermore, our results suggested that lupeol protected against MIRI-induced myocardial infarction through modulation of NF-[Formula: see text]B and Nrf2 signaling pathways. In summary, this study first clarified the cardioprotective effects of lupeol against I/R-induced myocardial infarction in rats, which could be due to its anti-oxidant, anti-inflammatory, and anti-apoptotic activities. Our study also highlighted a mechanism of NF-[Formula: see text]B and Nrf2 signaling, through which lupeol could be a promising agent in protecting against I/R-induced myocardial infarction.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44741359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Quercetin Mitigates Cisplatin-Induced Oxidative Damage and Apoptosis in Cardiomyocytes through Nrf2/HO-1 Signaling Pathway. 槲皮素通过Nrf2/HO-1信号通路减轻顺铂诱导的心肌细胞氧化损伤和凋亡。
Pub Date : 2022-06-04 DOI: 10.1142/S0192415X22500537
Shih-Hao Wang, Kun-Ling Tsai, Wan-Ching Chou, Hui-Ching Cheng, Yu-Ting Huang, H. Ou, Yun-Ching Chang
Cisplatin is massively used to treat solid tumors. However, several severe adverse effects, such as cardiotoxicity, are obstacles to its clinical application. Cardiotoxicity may lead to congestive heart failure and even sudden cardiac death in patients receiving cisplatin. Therefore, finding a novel therapeutic strategy for the prevention of cisplatin-induced cardiotoxicity is urgent. Quercetin is a flavonol compound that can be found in dietary fruits and vegetables. The antioxidant function and anti-inflammatory capacity of quercetin have been reported. However, whether quercetin could protect against cisplatin-caused apoptosis and cellular damage in cardiomyocytes is still unclear. H9c2 cardiomyocytes were treated with cisplatin (40 [Formula: see text] M) for 24 h to induce cellular damage with or without quercetin pretreatment. We found that quercetin activates Nrf2 and HO-1 expression, thereby mitigating cisplatin-caused cytotoxicity in H9c2 cells. Quercetin also increases SOD levels, maintains mitochondrial function, and reduces oxidative stress under cisplatin stimulation. Quercetin attenuates cisplatin-induced apoptosis and inflammation in H9c2 cardiomyocytes; however, these cytoprotective effects were diminished by silencing Nrf2 and HO-1. In conclusion, this study reports that quercetin has the potential to antagonize cisplatin-caused cardiotoxicity by reducing ROS-mediated mitochondrial damage and inflammation via the Nrf2/HO-1 and p38MAPK/NF-[Formula: see text]Bp65/IL-8 signaling pathway. This study provided the theoretical basis and experimental proof for the clinical application of quercetin as a new effective strategy to relieve chemotherapy-induced cardiotoxicity.
顺铂被大量用于治疗实体瘤。然而,一些严重的不良反应,如心脏毒性,是其临床应用的障碍。心脏毒性可能导致接受顺铂治疗的患者充血性心力衰竭,甚至心源性猝死。因此,迫切需要找到一种新的治疗策略来预防顺铂诱导的心脏毒性。槲皮素是一种黄酮醇化合物,可在膳食水果和蔬菜中找到。槲皮素具有抗氧化和抗炎作用。然而,槲皮素是否能预防顺铂引起的心肌细胞凋亡和细胞损伤尚不清楚。用顺铂(40[公式:见正文]M)处理H9c2心肌细胞24小时,以在有或没有槲皮素预处理的情况下诱导细胞损伤。我们发现槲皮素激活Nrf2和HO-1的表达,从而减轻顺铂引起的H9c2细胞的细胞毒性。槲皮素还能提高SOD水平,维持线粒体功能,并减少顺铂刺激下的氧化应激。槲皮素减轻顺铂诱导的H9c2心肌细胞凋亡和炎症反应;然而,这些细胞保护作用通过沉默Nrf2和HO-1而减弱。总之,本研究报告称,槲皮素有可能通过Nrf2/HO-1和p38MAPK/NF-[公式:见正文]Bp65/IL-8信号通路减少ROS介导的线粒体损伤和炎症,从而对抗顺铂引起的心脏毒性。本研究为槲皮素作为一种新的缓解化疗所致心脏毒性的有效策略在临床上的应用提供了理论依据和实验依据。
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引用次数: 9
Smilax china Polyphenols Stimulate Browning via [Formula: see text]3-Adrenergic Receptor/AMP-Activated Protein Kinase [Formula: see text] Signaling Pathway in 3T3-L1 Adipocytes. Smilax china多酚通过【公式:见正文】3-肾上腺素能受体/AMP激活蛋白激酶【公式:参见正文】3T3-L1脂肪细胞中的信号通路刺激褐变。
Pub Date : 2022-05-31 DOI: 10.1142/S0192415X22500550
Liz Kong, Meng Xu, Licong Yang, Shanshan Liu, G. Zheng
The aim of this study is to investigate the molecular mechanism of Smilax china L. polyphenols (SCLPs) in enhancing lipid metabolism and stimulating browning to reduce lipid accumulation in 3T3-L1 adipocytes. SCLP treatment obviously decreased lipid content in a dose-dependent manner (10-40 [Formula: see text]g/mL) in adipocytes. SCLP treatment cooperated with noradrenalin to increase lipolysis. SCLPs reduced the gene expressions of C/EBP[Formula: see text] and Ap2and enhanced the expressions of ACO, CPT, pHSL/HSL, ATGL, and PKA in adipocytes. Furthermore, SCLPs increased mRNA and protein expressions of brown adipocyte-specific factors (UCP-1, PRDM16, PGC-1[Formula: see text], and PPAR[Formula: see text] and mRNA expressions of beige adipocyte-specific markers (CD137, Tbx1, and Tmem26) in 3T3-L1 adipocytes, as well as mitochondrial biogenesis genes (Nrf1 and Tfam). In addition, according to the immunofluorescence staining, the mitochondria number was increased by SCLP. Moreover, [Formula: see text]3-AR or AMPK agonist synergistic SCLPs enhanced the expressions of UCP-1, PRDM16, and PGC-1[Formula: see text]. While [Formula: see text]3-AR or AMPK antagonist significantly decreased the expressions of these brown adipocyte-specific factors, SCLP treatment inhibited the effect of antagonist to improve the expression of UCP-1, PRDM16, and PGC-1[Formula: see text]. These results indicated that SCLPs may regulate lipid metabolism and stimulate browning via the [Formula: see text]3-AR/AMPK[Formula: see text] signaling pathway. Thus, SCLPs likely have potential therapeutic effects on obesity.
本研究旨在探讨菝葜多酚(SCLPs)在3T3-L1脂肪细胞中促进脂质代谢、促进褐变、减少脂质积累的分子机制。SCLP处理明显降低脂肪细胞的脂质含量,呈剂量依赖性(10-40 g/mL)。SCLP联合去甲肾上腺素可促进脂肪分解。SCLPs降低了脂肪细胞中C/EBP[公式:见文]和ap2的基因表达,提高了ACO、CPT、pHSL/HSL、ATGL和PKA的表达。此外,SCLPs增加了褐色脂肪细胞特异性因子(UCP-1、PRDM16、PGC-1[公式:见文本]和PPAR[公式:见文本]的mRNA和蛋白表达,以及3T3-L1脂肪细胞中褐色脂肪细胞特异性标志物(CD137、Tbx1和Tmem26)的mRNA表达,以及线粒体生物发生基因(Nrf1和Tfam)。此外,免疫荧光染色显示,SCLP使线粒体数量增加。此外,3-AR或AMPK激动剂增效的SCLPs增强了UCP-1、PRDM16和PGC-1的表达[公式:见文本]。3-AR或AMPK拮抗剂显著降低了这些棕色脂肪细胞特异性因子的表达,而SCLP处理抑制了拮抗剂提高UCP-1、PRDM16和pcc -1表达的作用[公式:见文本]。这些结果表明,SCLPs可能通过3-AR/AMPK信号通路调节脂质代谢,刺激褐变。因此,SCLPs可能对肥胖有潜在的治疗作用。
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引用次数: 1
期刊
The American journal of Chinese medicine
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