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Natural Products in the Modulation of Farnesoid X Receptor Against Nonalcoholic Fatty Liver Disease. 天然产品在调节法恩类 X 受体防治非酒精性脂肪肝中的作用
Pub Date : 2024-01-01 Epub Date: 2024-03-14 DOI: 10.1142/S0192415X24500137
Jing Wang, Na Yang, Yu Xu

Nonalcoholic fatty liver disease (NAFLD) is a global health concern with a high prevalence and increasing economic burden, but official medicine remains unavailable. Farnesoid X receptor (FXR), a nuclear receptor member, is one of the most promising drug targets for NAFLD therapy that plays a crucial role in modulating bile acid, glucose, and lipid homeostasis, as well as inhibits hepatic inflammation and fibrosis. However, the rejection of the FXR agonist, obecholic acid, by the Food and Drug Administration for treating hepatic fibrosis raises a question about the functions of FXR in NAFLD progression and the therapeutic strategy to be used. Natural products, such as FXR modulators, have become the focus of attention for NAFLD therapy with fewer adverse reactions. The anti-NAFLD mechanisms seem to act as FXR agonists and antagonists or are involved in the FXR signaling pathway activation, indicating a promising target of FXR therapeutic prospects using natural products. This review discusses the effective mechanisms of FXR in NAFLD alleviation, and summarizes currently available natural products such as silymarin, glycyrrhizin, cycloastragenol, berberine, and gypenosides, for targeting FXR, which can facilitate development of naturally targeted drug by medicinal specialists for effective treatment of NAFLD.

非酒精性脂肪肝(NAFLD)是一个全球关注的健康问题,发病率很高,经济负担日益加重,但官方药物仍然缺乏。法尼类固醇 X 受体(FXR)是一种核受体,是治疗非酒精性脂肪肝最有希望的药物靶点之一,它在调节胆汁酸、葡萄糖和脂质平衡以及抑制肝脏炎症和纤维化方面发挥着至关重要的作用。然而,食品药品管理局拒绝将 FXR 激动剂顺胆酸用于治疗肝纤维化,这引发了人们对 FXR 在非酒精性脂肪肝进展过程中的功能以及治疗策略的疑问。天然产品(如 FXR 调节剂)已成为非酒精性脂肪肝治疗中不良反应较少的关注焦点。抗非酒精性脂肪肝的机制似乎可作为 FXR 激动剂和拮抗剂,或参与 FXR 信号通路的激活,这表明利用天然产品靶向治疗 FXR 前景广阔。本综述探讨了 FXR 在缓解非酒精性脂肪肝中的有效机制,并总结了水飞蓟素、甘草苷、环黄芪醇、小檗碱和石膏苷等目前可用于靶向 FXR 的天然产物,这有助于药学专家开发天然靶向药物,以有效治疗非酒精性脂肪肝。
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引用次数: 0
Insight of Chinese Herbal Medicine in Treating Osteoporosis: Achievements from 2013 to 2023. 中药治疗骨质疏松症的启示:2013年至2023年的成就。
Pub Date : 2024-01-01 Epub Date: 2024-08-28 DOI: 10.1142/S0192415X24500526
Mingshuai Tan, Qiang Li, Bencheng Yang, Sihan Wang, Ze Chen

Osteoporosis is the most common bone metabolic disease, and it is becoming increasingly common as the global population ages. Osteoporosis and its complications, such as fractures and pain, negatively affect patient quality of life and easily lead to disability, placing enormous burdens on society. Although several anti-osteoporosis drugs are currently available, many adverse reactions have been observed during the long-term application of these drugs. Therefore, safer and more useful medications are urgently needed to replace those currently available. Chinese herbal medicine has been extensively used to treat osteoporosis, and the current literature confirms that such medicines have anti-osteoporosis effects, are safe, and have minimal side effects. Thus, Chinese herbal medicines are natural alternatives to pharmaceutical approaches to treating osteoporosis, and these medicines must be further developed and utilized. In this article, we review the mechanisms underlying the anti-osteoporosis effects of single herbal extracts and traditional Chinese medicine (TCM) formulas that have been elucidated since 2013, providing key evidence and support for future research on the anti-osteoporosis effects of Chinese herbal medicines. In addition, due to the complexity of the ingredients in Chinese herbal medicine, more thorough investigations are needed to determine the specific ingredients that are effective in osteoporosis treatment. Therefore, identifying the effective ingredients of Chinese herbal medicines will be a necessary focus in laboratory research and clinical application.

骨质疏松症是最常见的骨代谢疾病,随着全球人口的老龄化,骨质疏松症正变得越来越常见。骨质疏松症及其并发症,如骨折和疼痛,对患者的生活质量造成负面影响,并容易导致残疾,给社会带来巨大负担。虽然目前已有多种抗骨质疏松症药物,但在长期应用这些药物的过程中发现了许多不良反应。因此,迫切需要更安全、更有效的药物来替代现有药物。中药已被广泛用于治疗骨质疏松症,目前的文献证实,中药具有抗骨质疏松症的作用,而且安全、副作用小。因此,中药是治疗骨质疏松症的药物疗法的天然替代品,必须进一步开发和利用这些药物。本文回顾了 2013 年以来已阐明的单味中药提取物和传统中药配方的抗骨质疏松症作用机制,为今后研究中药的抗骨质疏松症作用提供关键证据和支持。此外,由于中药成分的复杂性,还需要进行更深入的研究,以确定对骨质疏松症治疗有效的具体成分。因此,确定中药的有效成分将是实验室研究和临床应用的一个必要重点。
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引用次数: 0
Chinese Medicine-Derived Salvianolic Acid B for Disease Therapy: A Scientometric Study. 用于疾病治疗的中药丹酚酸 B:科学计量学研究
Pub Date : 2024-01-01 Epub Date: 2024-08-29 DOI: 10.1142/S0192415X2450054X
Meina Zhao, Fei Mu, Rui Lin, Kai Gao, Wei Zhang, Xingru Tao, Dong Xu, Jingwen Wang

Salvianolic acid B (SalB), among the most abundant bioactive polyphenolic compounds found in Salvia miltiorrhiza Bge., exerts therapeutic and protective effects against various diseases. Although some summaries of the activities of SalB exist, there is lack of a scientometric and in-depth review regarding disease therapy. In this review, scientometrics was employed to analyze the number of articles, publication trends, countries, institutions, keywords, and highly cited papers pertaining to SalB research. The scientometric findings showed that SalB exerts excellent protective effects on the heart, lungs, liver, bones, and brain, along with significant therapeutic effects against atherosclerosis (AS), Alzheimer's disease (AD), liver fibrosis, diabetes, heart/brain ischemia, and osteoporosis, by regulating signaling pathways and acting on specific molecular targets. Moreover, this review delves into in-depth insights and perspectives, such as the utilization of SalB in combination with other drugs, the validation of molecular mechanisms and targets, and the research and development of novel drug carriers and dosage forms. In conclusion, this review aimed to offer a comprehensive scientometric analysis and in-depth appraisal of SalB research, encompassing both present achievements and future prospects, thereby providing a valuable resource for the clinical application and therapeutic exploitation of SalB.

丹酚酸 B(SalB)是丹参(Salvia miltiorrhiza Bge.)中最丰富的生物活性多酚化合物之一,对多种疾病具有治疗和保护作用。虽然有一些关于丹参酸活性的总结,但缺乏关于疾病治疗的科学计量学和深入综述。本综述采用科学计量学方法分析了与盐肤木研究相关的文章数量、发表趋势、国家、机构、关键词和高被引论文。科学计量学研究结果表明,SalB 通过调节信号通路和作用于特定分子靶点,对心脏、肺部、肝脏、骨骼和大脑具有良好的保护作用,对动脉粥样硬化(AS)、阿尔茨海默病(AD)、肝纤维化、糖尿病、心脏/脑缺血和骨质疏松症具有显著的治疗效果。此外,本综述还深入探讨了 SalB 与其他药物的联合应用、分子机制和靶点的验证以及新型药物载体和剂型的研究与开发等问题。总之,本综述旨在对 SalB 的研究进行全面的科学计量分析和深入评价,既包括目前的成就,也包括未来的前景,从而为 SalB 的临床应用和治疗开发提供宝贵的资源。
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引用次数: 0
Schisandrol A, the Major Active Constitute in Schisandra chinensis: A Review of Its Preparation, Biological Activities, and Pharmacokinetics Analysis. 五味子中的主要活性成分五味子醇 A:五味子中的主要活性成分五味子醇 A:制备、生物活性和药代动力学分析综述。
Pub Date : 2024-01-01 Epub Date: 2024-05-08 DOI: 10.1142/S0192415X24500290
Ying Wu, Chao Ding, Chenwang Liu, Linwei Dan, Haonan Xu, Xinzhuo Li, Yuze Li, Xiaomei Song, Dongdong Zhang

Schisandra chinensis (S. chinensis) has a long history as a traditional Chinese medicine that is astringent, beneficial to vital energy, tonifies the kidney, tranquilizes the heart, etc. Significantly, Schisandrol A (SA) is extracted from S. chinensis and shows surprising and satisfactory biological activity, including anti-inflammatory, hepatoprotective, cardiovascular protection, and antitumor properties, among others. SA has a more pronounced protective effect on central damaged nerves among its numerous pharmacological effects, improving neurodegenerative diseases such as Alzheimer's and Parkinson's through the protection of damaged nerve cells and the enhancement of anti-oxidant capacity. Pharmacokinetic studies have shown that SA has a pharmacokinetic profile with a rapid absorption, wide distribution, maximal concentration in the liver, and primarily renal excretion. However, hepatic and intestinal first-pass metabolism can affect SA's bioavailability. In addition, the content of SA, as an index component of S. chinensis Pharmacopoeia, should not be less than 0.40%, and the content of SA in S. chinensis compound formula was determined with the help of high-performance liquid chromatography (HPLC), which is a stable and reliable method, and it can lay a foundation for the subsequent quality control. Therefore, this paper systematically reviews the preparation, pharmacological effects, pharmacokinetic properties, and content determination of SA with the goal of updating and deepening the understanding of SA, as well as providing a theoretical basis for the study of SA at a later stage.

五味子是一种历史悠久的传统中药,具有收敛、益气、补肾、宁心安神等功效。值得注意的是,从五味子中提取的五味子甲(SA)显示出令人惊讶和满意的生物活性,包括抗炎、保肝、保护心血管和抗肿瘤等特性。在众多药理作用中,SA 对中枢受损神经的保护作用更为明显,通过保护受损神经细胞和增强抗氧化能力,可改善阿尔茨海默氏症和帕金森氏症等神经退行性疾病。药代动力学研究表明,SA 的药代动力学特征是吸收快、分布广,在肝脏中浓度最高,主要经肾脏排泄。不过,肝脏和肠道的首过代谢会影响 SA 的生物利用度。此外,SA 作为《金银花药典》中的指标成分,其含量应不低于 0.40%,而金银花复方中 SA 的含量采用高效液相色谱法(HPLC)测定,该方法稳定可靠,可为后续的质量控制奠定基础。因此,本文系统地综述了SA的制备、药理作用、药代动力学特性及含量测定,旨在更新和加深对SA的认识,并为后期SA的研究提供理论依据。
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引用次数: 0
Flavonoids Derived from Chinese Medicine: Potential Neuroprotective Agents. 从中药中提取的黄酮类化合物:潜在的神经保护剂
Pub Date : 2024-01-01 Epub Date: 2024-09-30 DOI: 10.1142/S0192415X24500630
Jinhua Li, Ye Yu, Yanjie Zhang, Yilin Zhou, Shuxian Ding, Shuze Dong, Sainan Jin, Qin Li

Due to their complex pathological mechanisms, neurodegenerative diseases have brought great challenges to drug development and clinical treatment. Studies have shown that many traditional Chinese medicines have neuroprotective pharmacological activities such as anti-inflammatory and anti-oxidation properties and have certain effects on improving the symptoms of neurodegenerative diseases and delaying disease progression. Flavonoids are the main active components of many traditional Chinese medicines for the treatment of neurodegenerative diseases. These compounds have a wide range of biological activities, including anti-inflammatory, anti-oxidative stress, regulation of autophagy balance, inhibition of apoptosis, and promotion of neuronal regeneration. This paper focuses on the neuroprotective effects of six common flavonoids: quercetin, rutin, luteolin, kaempferol, baicalein, and puerarin. It then systematically reviews their characteristics, mechanisms, and key signaling pathways, summarizes the common characteristics and laws of their neuroprotective effects, and discusses the significance of strengthening the research on the neuroprotective effects of these compounds, aiming to provide reference for more research and drug development of these substances as neuroprotective drugs.

神经退行性疾病病理机制复杂,给药物研发和临床治疗带来了巨大挑战。研究表明,许多中药具有抗炎、抗氧化等神经保护药理活性,对改善神经退行性疾病症状、延缓疾病进展有一定作用。黄酮类化合物是许多治疗神经退行性疾病中药的主要活性成分。这些化合物具有广泛的生物活性,包括抗炎、抗氧化应激、调节自噬平衡、抑制细胞凋亡和促进神经元再生。本文重点研究了槲皮素、芦丁、木犀草素、山奈酚、黄芩苷和葛根素这六种常见黄酮类化合物的神经保护作用。然后系统综述了它们的特点、作用机制和关键信号通路,总结了它们神经保护作用的共同特点和规律,探讨了加强这些化合物神经保护作用研究的意义,旨在为更多地研究和开发这些物质作为神经保护药物提供参考。
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引用次数: 0
Honokiol Exhibits Anti-Tumor Effects in Breast Cancer by Modulating the miR-148a-5p-CYP1B1 Axis. Honokiol通过调节miR-148a-5p-CYP1B1轴对乳腺癌具有抗肿瘤作用
Pub Date : 2024-01-01 Epub Date: 2024-09-30 DOI: 10.1142/S0192415X24500721
Xuejiao Han, Yuan Cheng, Zedong Jiang, Aqu Alu, Xuelei Ma

Breast cancer (BC) is the most frequently diagnosed malignancy in female patients. There is a significant lack of therapeutic strategies for BC, particularly triple-negative breast cancer (TNBC). Honokiol (HNK), a lignin extracted from the Magnolia genus plant, has demonstrated numerous pharmacological effects. Therefore, this study aims to investigate the antitumor effect of HNK on BC cells and employ high-throughput sequencing to elucidate its potential mechanism. We found that HNK significantly inhibited proliferation and induced apoptosis on BC cell lines in a dose-dependent manner. Moreover, HNK treatment suppressed migration and colony formation and initiated the intrinsic apoptotic pathway specifically in MDA-MB-231 cells. High-throughput sequencing and bioinformatics analysis revealed that miR-148a-5p expression was significantly up-regulated, whereas CYP1B1 expression was down-regulated following HNK treatment. Importantly, survival analysis based on TCGA database showed high miR-148a-5p expression was correlated with a better prognosis for BC patients. Inhibition of miR-148a-5p by inhibitor not only increased cell viability but also attenuated apoptosis induced by HNK. Finally, a strong synergistic effect between HNK and paclitaxel was observed in vitro. In conclusion, our study validated the antitumor efficacy of HNK against human BC cells and elucidated its underlying mechanism through high-throughput sequencing, thereby providing compelling evidence for further exploration of the potential clinical application of HNK towards the treatment of BC.

乳腺癌(BC)是女性患者中最常确诊的恶性肿瘤。针对乳腺癌,尤其是三阴性乳腺癌(TNBC)的治疗策略非常缺乏。Honokiol(HNK)是从木兰科植物中提取的一种木质素,具有多种药理作用。因此,本研究旨在研究HNK对BC细胞的抗肿瘤作用,并采用高通量测序技术阐明其潜在机制。我们发现,HNK能以剂量依赖的方式明显抑制BC细胞株的增殖并诱导其凋亡。此外,HNK还能抑制MDA-MB-231细胞的迁移和集落形成,并启动其内在凋亡途径。高通量测序和生物信息学分析表明,HNK 处理后,miR-148a-5p 的表达明显上调,而 CYP1B1 的表达下调。重要的是,基于TCGA数据库的生存分析表明,miR-148a-5p的高表达与BC患者较好的预后相关。抑制剂抑制 miR-148a-5p 不仅能提高细胞活力,还能减轻 HNK 诱导的细胞凋亡。最后,在体外观察到 HNK 与紫杉醇之间有很强的协同作用。总之,我们的研究验证了HNK对人类BC细胞的抗肿瘤功效,并通过高通量测序阐明了其潜在机制,从而为进一步探索HNK治疗BC的潜在临床应用提供了有力证据。
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引用次数: 0
Ginsenoside Rh4 Ameliorates Cisplatin-Induced Intestinal Toxicity via PGC-1[Formula: see text]-Mediated Mitochondrial Autophagy and Apoptosis Pathways. 人参皂苷 Rh4 通过 PGC-1[配方:见正文]介导的线粒体自噬和细胞凋亡途径改善顺铂诱导的肠道毒性
Pub Date : 2024-01-01 Epub Date: 2024-11-19 DOI: 10.1142/S0192415X24500848
Wei Liu, Meng Sun, Wen-Ting Wang, Jian Song, Chun-Mei Wang, Neng-Yan Mou, Tian-Qi Shao, Zhi-Hong Zhang, Meng-Yang Wang, Hai-Ming Sun

Cisplatin-evoked profound gastrointestinal symptomatology is one of the most common side effects of chemotherapy drugs, causing further gastrointestinal cell and intestinal mucosal injury. Ginsenoside Rh4 (G-Rh4), an active component extracted from red ginseng, possesses beneficial anti-oxidative and anti-apoptosis effects. This study aimed to assess the effectiveness of pharmacological intervention with G-Rh4 mitigating intestinal toxicity evoked by cisplatin in a murine model and in IEC-6 cells in vitro. Following oral administration for 10 days, G-Rh4 (10[Formula: see text]mg/kg and 20[Formula: see text]mg/kg) significantly increased the indicators of diamine oxidase (DAO) affected by cisplatin (20[Formula: see text]mg/kg) in mice, and histopathological analysis further indicated that G-Rh4 could effectively improve intestinal tissue morphology, as well as the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 [Formula: see text] (PGC-1[Formula: see text] pathway and autophagy-related proteins. Moreover, in vitro experiments demonstrated that G-Rh4 exerted a concentration-dependent increase in cell viability, while also inhibiting cytotoxicity and abnormal rise of reactive oxygen species (ROS). Notably, ROS also activate PGC-1[Formula: see text] protein and mediate the occurrence of mitochondrial autophagy and apoptosis pathways. The molecular docking approach was employed to dock G-Rh4 with PGC-1[Formula: see text] and AMPK, revealing a binding energy of [Formula: see text]7.3[Formula: see text]kcal/mol and [Formula: see text]8.1[Formula: see text]kcal/mol and indicating a tight interaction between the components and the target. G-Rh4 could reduce the expression of autophagy-related protein p62/p53, reduce the accumulation of autophagy products, and promote the flow of autophagy. In conclusion, G-Rh4 exerted protective effects against cisplatin-induced intestinal toxicity, at least partially through PGC-1[Formula: see text]-mediated autophagy and apoptosis.

顺铂引起的严重胃肠道症状是化疗药物最常见的副作用之一,会进一步造成胃肠道细胞和肠粘膜损伤。人参皂苷 Rh4(G-Rh4)是从红参中提取的一种活性成分,具有抗氧化和抗细胞凋亡的作用。本研究旨在评估在小鼠模型和体外 IEC-6 细胞中使用 G-Rh4 进行药物干预对减轻顺铂引起的肠道毒性的效果。口服 G-Rh4(10[式:见正文]mg/kg 和 20[式:见正文]mg/kg)10 天后,顺铂(20[式:见正文]mg/kg)对二胺氧化酶(DAO)指标的影响显著增加:组织病理学分析进一步表明,G-Rh4 可有效改善小鼠肠道组织形态,以及过氧化物酶体增殖激活受体-γ 辅激活因子 1[式:见正文](PGC-1[式:见正文]通路和自噬相关蛋白的表达。此外,体外实验表明,G-Rh4 还能依赖浓度提高细胞活力,同时抑制细胞毒性和活性氧(ROS)的异常升高。值得注意的是,ROS 还能激活 PGC-1[式中:见正文]蛋白,并介导线粒体自噬和细胞凋亡途径的发生。采用分子对接法将 G-Rh4 与 PGC-1[式:见正文]和 AMPK 对接,发现其结合能分别为[式:见正文]7.3[式:见正文]kcal/mol 和[式:见正文]8.1[式:见正文]kcal/mol,表明该成分与目标之间存在紧密的相互作用。G-Rh4可以降低自噬相关蛋白p62/p53的表达,减少自噬产物的积累,促进自噬的流动。总之,G-Rh4对顺铂诱导的肠毒性具有保护作用,至少部分作用是通过PGC-1[式:见正文]介导的自噬和细胞凋亡实现的。
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引用次数: 0
Liquiritigenin, an Active Ingredient of Liquorice, Alleviates Acute Kidney Injury by VKORC1-Mediated Ferroptosis Inhibition. 甘草中的一种活性成分--甘草苷能通过 VKORC1 介导的铁氧化酶抑制缓解急性肾损伤
Pub Date : 2024-01-01 Epub Date: 2024-08-28 DOI: 10.1142/S0192415X24500599
Run-Zhi Guo, Jia Li, Shao-Kang Pan, Ming-Yang Hu, Lin-Xiao Lv, Qi Feng, Ying-Jin Qiao, Jia-Yu Duan, Dong-Wei Liu, Zhang-Suo Liu

Acute kidney injury (AKI) is a major public health problem worldwide that still lacks effective treatments. Recent studies have suggested that ferroptosis is a key mediator of AKI due to its activation of lipid peroxidation. Therefore, we hypothesized that antiferroptosis agents might be a novel potential therapeutic strategy for AKI. Herein, we demonstrated that liquiritigenin (LG), an active ingredient of liquorice, improves renal function by inhibiting vitamin K epoxide reductase complex subunit 1 (VKORC1)-mediated ferroptosis, both in vivo and in vitro. In a folic acid-induced murine AKI model, after a single pre-treatment intravenous injection, LG markedly alleviated the loss of renal function through suppressing ferroptosis induced by iron accumulation. LG prevented mitochondrial morphological changes and upregulated glutathione and glutathione peroxidase 4 levels, while downregulating malonaldehyde and divalent iron levels. An in vitro RNA-sequence analysis suggested that the protective role of LG may involve upregulation of VKORC1. Moreover, knockdown of VKORC1 diminished the renal protective and antiferroptosis roles of LG. Collectively, our findings demonstrated that LG protected against AKI by inhibiting VKORC1-mediated ferroptosis. This suggests that inhibiting ferroptosis might be a novel therapeutic approach in the future.

急性肾损伤(AKI)是全球主要的公共卫生问题,目前仍缺乏有效的治疗方法。最近的研究表明,铁变态反应是急性肾损伤的一个关键介质,因为它激活了脂质过氧化反应。因此,我们推测抗铁蛋白沉积药物可能是治疗 AKI 的一种新的潜在治疗策略。在此,我们证明了甘草的活性成分甘草苷(liquiritigenin,LG)可通过抑制维生素 K 环氧化物还原酶复合物亚基 1(VKORC1)介导的体内和体外铁突变来改善肾功能。在叶酸诱导的小鼠 AKI 模型中,经过单次预处理静脉注射后,LG 通过抑制铁蓄积诱导的铁蛋白沉积,明显减轻了肾功能的丧失。LG 可防止线粒体形态学变化,上调谷胱甘肽和谷胱甘肽过氧化物酶 4 的水平,同时下调丙二醛和二价铁的水平。体外 RNA 序列分析表明,LG 的保护作用可能涉及 VKORC1 的上调。此外,敲除 VKORC1 会削弱 LG 的肾脏保护和抗铁细胞减少作用。总之,我们的研究结果表明,LG 可通过抑制 VKORC1 介导的铁蛋白沉积来防止 AKI。这表明,抑制铁突变可能是未来的一种新型治疗方法。
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引用次数: 0
Acupuncture: An Overview on Its Functions, Meridian Pathways and Molecular Mechanisms. 针灸:针灸的功能、经络路径和分子机制概述。
Pub Date : 2024-01-01 Epub Date: 2024-08-29 DOI: 10.1142/S0192415X24500496
Rong Han, Jinlian Hu

Recent research has extensively explored the intricate mechanisms that underlie the effectiveness of acupuncture, highlighting the importance of stimulating acupoints, the role of acupuncture techniques in managing diseases, and the interaction between meridian pathways and molecular processes. Studies have underscored the crucial role of acupuncture in activating neurons, modulating the immune system, and influencing vascular activity, all of which contribute significantly to its therapeutic benefits across a wide range of symptoms and conditions. Utilization of imaging modalities enables the identification of changes in cerebral blood flow, brain function, and regional glucose metabolism following acupuncture sessions. The interstitial fluid circulation network within meridians adheres to specific laws that facilitate the transportation of materials. Acupuncture initiates the release of neurotransmitters, neuropeptides, and immune factors, impacting pain perception, inflammation, and physiological functions. It influences the complex neuro-endocrine-immune network by activating pathways involving the nervous system, the hypothalamic-pituitary-adrenal axis, and immune responses. Moreover, acupuncture induces molecular modifications such as phosphorylation, methylation, and histone modification, leading to key molecular changes that ultimately result in anti-inflammatory effects and the regulation of immune responses.

最近的研究广泛探讨了针灸疗效的复杂机制,强调了刺激穴位的重要性、针灸技术在控制疾病中的作用以及经络通路与分子过程之间的相互作用。研究强调了针灸在激活神经元、调节免疫系统和影响血管活动方面的关键作用,所有这些都极大地促进了针灸对各种症状和病症的治疗效果。利用成像模式可以识别针灸治疗后脑血流量、脑功能和区域葡萄糖代谢的变化。经络内的体液间循环网络遵循特定的规律,有利于物质的运输。针灸可启动神经递质、神经肽和免疫因子的释放,影响痛觉、炎症和生理功能。针灸通过激活神经系统、下丘脑-垂体-肾上腺轴和免疫反应的途径,影响复杂的神经-内分泌-免疫网络。此外,针灸还能诱导磷酸化、甲基化和组蛋白修饰等分子改变,从而导致关键的分子变化,最终产生抗炎作用和免疫反应调节。
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引用次数: 0
Curcumin Analog L48H37 Induces Apoptosis in Human Oral Cancer Cells by Activating Caspase Cascades and Downregulating the Inhibitor of Apoptosis Proteins through JNK/p38 Signaling. 姜黄素类似物 L48H37 通过 JNK/p38 信号激活 Caspase 级联和下调凋亡抑制蛋白诱导人口腔癌细胞凋亡
Pub Date : 2024-01-01 Epub Date: 2024-03-14 DOI: 10.1142/S0192415X24500241
Chun-Wen Su, Shao-Hsuan Kao, Yi-Tzu Chen, Yi-Hsien Hsieh, Wei-En Yang, Meng-Ying Tsai, Chiao-Wen Lin, Shun-Fa Yang

L48H37 is a synthetic curcumin analog that has anticancer potentials. Here, we further explored the anticancer effect of L48H37 on oral cancer cells and its mechanistic acts. Cell cycle distribution was assessed using flow cytometric analysis. Apoptosis was elucidated by staining with PI/Annexin V and activation of the caspase cascade. Cellular signaling was explored using apoptotic protein profiling, Western blotting, and specific inhibitors. Our findings showed that L48H37 significantly reduced the cell viability of SCC-9 and HSC-3 cells, resulting in sub-G1 phase accumulation and increased apoptotic cells. Apoptotic protein profiling revealed that L48H37 increased cleaved caspase-3, and downregulated cellular inhibitor of apoptosis protein 1 (cIAP1) and X-linked inhibitor of apoptosis protein (XIAP) in SCC-9 cells, and the downregulated cIAP1 and XIAP in both oral cancer cells were also demonstrated by Western blotting. Meanwhile, L48H37 triggered the activation of caspases and mitogen-activated protein kinases (MAPKs). The involvement of c-Jun N-terminal kinase (JNK) and p38 MAPK (p38) in the L48H37-triggered apoptotic cascade in oral cancer cells was also elucidated by specific inhibitors. Collectively, these findings indicate that L48H37 has potent anticancer activity against oral cancer cells, which may be attributed to JNK/p38-mediated caspase activation and the resulting apoptosis. This suggests a potential benefit for L48H37 for the treatment of oral cancer.

L48H37 是一种具有抗癌潜力的合成姜黄素类似物。在此,我们进一步探讨了 L48H37 对口腔癌细胞的抗癌作用及其机理作用。细胞周期分布采用流式细胞分析法进行评估。通过 PI/Annexin V 染色和 caspase cascade 激活来阐明细胞凋亡。利用凋亡蛋白图谱、Western 印迹和特异性抑制剂探索了细胞信号传导。我们的研究结果表明,L48H37 能显著降低 SCC-9 和 HSC-3 细胞的存活率,导致亚 G1 期积累和凋亡细胞增加。凋亡蛋白图谱显示,L48H37增加了SCC-9细胞中裂解的caspase-3,下调了细胞凋亡抑制蛋白1(cIAP1)和X-连锁凋亡抑制蛋白(XIAP)。同时,L48H37 引发了 Caspases 和丝裂原活化蛋白激酶(MAPKs)的活化。特异性抑制剂也阐明了 c-Jun N 端激酶(JNK)和 p38 MAPK(p38)参与 L48H37 触发的口腔癌细胞凋亡级联反应。总之,这些研究结果表明,L48H37 对口腔癌细胞具有很强的抗癌活性,这可能归因于 JNK/p38 介导的 caspase 激活和由此产生的细胞凋亡。这表明 L48H37 有助于治疗口腔癌。
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The American journal of Chinese medicine
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