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Cathepsin B maturation plays a critical role in leptin-induced hepatic cancer cell growth through activation of NLRP3 inflammasomes 组织蛋白酶B成熟通过激活NLRP3炎性小体在瘦素诱导的肝癌细胞生长中起关键作用
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-03-11 DOI: 10.1007/s12272-023-01437-2
ThiKem Nguyen, Raut Pawan Kumar, Pil-Hoon Park

Leptin, an adipose tissue-derived hormone, exhibits potent tumor promoting effects through various mechanisms. Cathepsin B, a member of the lysosomal cysteine proteases, has been shown to modulate the growth of cancer cells. In this study, we have investigated the role of cathepsin B signaling in leptin-induced hepatic cancer growth. Leptin treatment caused significant increase in the levels of active cathepsin B through the axis of endoplasmic reticulum stress and autophagy induction without significant effects on pre- and pro-forms of cathepsin B. Interestingly, inhibition of cathepsin B signaling by gene silencing or treatment with a selective pharmacological inhibitor (CA-074) prevented leptin-enhanced viability of hepatic cancer cell and suppressed progression of cell cycle, indicating the critical role of cathepsin B in leptin-induced hepatic cancer growth. We have further observed that maturation of cathepsin B is required for NLRP3 inflammasomes activation, which is implicated in the growth of hepatic cancer cell. The crucial roles of cathepsin B maturation in leptin-induced hepatic cancer growth and NLRP3 inflammasomes activation were confirmed in an in vivo HepG2 tumor xenograft model. Taken together, these results demonstrate that cathepsin B signaling plays a pivotal role in leptin-induced hepatic cancer cell growth by activating NLRP3 inflammasomes.

瘦素是一种脂肪组织来源的激素,通过多种机制显示出强大的促肿瘤作用。组织蛋白酶B是溶酶体半胱氨酸蛋白酶的一员,已被证明可以调节癌细胞的生长。在这项研究中,我们研究了组织蛋白酶B信号在瘦素诱导的肝癌生长中的作用。瘦素治疗通过内质网应激轴和自噬诱导引起活性组织蛋白酶B水平的显著增加,而对组织蛋白酶B的前和前形态没有显著影响。有趣的是,通过基因沉默或选择性药理抑制剂(CA-074)治疗来抑制组织蛋白酶B信号传导,阻止了瘦素增强的肝癌细胞活力和抑制细胞周期的进展。表明组织蛋白酶B在瘦素诱导的肝癌生长中起关键作用。我们进一步观察到组织蛋白酶B的成熟是NLRP3炎性小体激活所必需的,这与肝癌细胞的生长有关。在体内HepG2肿瘤异种移植模型中证实了组织蛋白酶B成熟在瘦素诱导的肝癌生长和NLRP3炎性体激活中的关键作用。综上所述,这些结果表明,组织蛋白酶B信号通过激活NLRP3炎症小体在瘦素诱导的肝癌细胞生长中起关键作用。
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引用次数: 1
Anti-fibrotic effect of aurocyanide, the active metabolite of auranofin 金糠蛋白的活性代谢物金糠氰的抗纤维化作用
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-03-10 DOI: 10.1007/s12272-023-01438-1
Hyun Young Kim, Undarmaa Otgontenger, Jun-Woo Kim, Young Joo Lee, Sang-Bum Kim, Sung Chul Lim, Young-Mi Kim, Keon Wook Kang

Drug repositioning has gained significant attention over the past several years. The anti-rheumatoid arthritis drug auranofin has been investigated for the treatment of other diseases, including liver fibrosis. Because auranofin is rapidly metabolized, it is necessary to identify the active metabolites of auranofin that have detectable levels in the blood and reflect its therapeutic effects. In the present study, we investigated whether aurocyanide as an active metabolite of auranofin, can be used to evaluate the anti-fibrotic effects of auranofin. Incubation of auranofin with liver microsomes showed that auranofin was susceptible to hepatic metabolism. Previously, we found that the anti-fibrotic effects of auranofin are mediated via system xc-dependent inhibition of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome. Therefore, we tried to identify active metabolites of auranofin based on their inhibitory effects on system xc and NLRP3 inflammasome in bone marrow-derived macrophages. Among the seven candidate metabolites, 1-thio-β-D-glycopyrano-sato-S-(triethyl-phosphine)-gold(I) and aurocyanide potently inhibited system xc and NLRP3 inflammasome. A pharmacokinetics study on mice detected significant plasma levels of aurocyanide after auranofin administration. Oral administration of aurocyanide significantly prevented thioacetamide-induced liver fibrosis in mice. Moreover, the in vitro anti-fibrotic effects of aurocyanide were assessed in LX-2 cells, where aurocyanide significantly decreased the migratory ability of the cells. In conclusion, aurocyanide is metabolically stable and detectable in plasma, and has inhibitory effects on liver fibrosis, suggesting that it is a potential marker of the therapeutic effects of auranofin.

药物重新定位在过去几年中获得了极大的关注。抗类风湿性关节炎药物金糠蛋白已被研究用于治疗其他疾病,包括肝纤维化。由于金糠磷脂代谢迅速,因此有必要鉴定血液中可检测水平并反映其治疗效果的金糠磷脂活性代谢物。在本研究中,我们研究了作为金糠蛋白活性代谢物的金氰化物是否可以用于评价金糠蛋白的抗纤维化作用。用肝微粒体孵育金糠蛋白表明,金糠蛋白对肝脏代谢敏感。先前,我们发现金糠蛋白的抗纤维化作用是通过对NOD-、LRR-和pyrin结构域蛋白3 (NLRP3)炎性体的系统xc依赖性抑制介导的。因此,我们试图根据其对骨髓源性巨噬细胞中系统xc -和NLRP3炎性体的抑制作用来鉴定金嘌呤的活性代谢物。在7种候选代谢物中,1-硫-β- d -glycopyrano-sato- s -(三乙基膦)-金(I)和金氰化物能有效抑制系统xc -和NLRP3炎性体。一项小鼠药代动力学研究发现,在给药后,小鼠血浆中有显著的金烷氰化物水平。口服金氰化物可显著预防硫代乙酰胺所致小鼠肝纤维化。此外,在LX-2细胞中评估了金氰化物的体外抗纤维化作用,金氰化物显著降低了细胞的迁移能力。综上所述,金氰化物代谢稳定,可在血浆中检测到,对肝纤维化有抑制作用,提示其可能是金氟芬治疗效果的潜在标志。
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引用次数: 2
Correction to: The multifaceted role of STAT3 pathway and its implication as a potential therapeutic target in oral cancer STAT3通路的多方面作用及其作为口腔癌潜在治疗靶点的意义
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-03-07 DOI: 10.1007/s12272-023-01434-5
Elina Khatoon, Mangala Hegde, Aviral Kumar, Uzini Devi Daimary, Gautam Sethi, Anupam Bishayee, Ajaikumar B. Kunnumakkara
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引用次数: 0
Antibody–drug conjugates and bispecific antibodies targeting cancers: applications of click chemistry 针对癌症的抗体-药物偶联物和双特异性抗体:点击化学的应用
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-03-06 DOI: 10.1007/s12272-023-01433-6
Yeji Hong, Su-Min Nam, Aree Moon

Engineering approaches using antibody drug conjugates (ADCs) and bispecific antibodies (bsAbs) are designed to overcome the limitations of conventional chemotherapies and therapeutic antibodies such as drug resistance and non-specific toxicity. Cancer immunotherapies have been shown to be clinically successful with checkpoint blockade and chimeric antigen receptor T cell therapy; however, overactive immune systems still represent a major problem. Given the complexity of a tumor environment, it would be advantageous to have a strategy targeting two or more molecules. We highlight the necessity and importance of a multi-target platform strategy against cancer. Approximately 400 ADCs and over 200 bsAbs are currently being clinically developed for several indications, with promising signs of therapeutic activity. ADCs include antibodies that recognize tumor antigens, linkers that stably connect drugs, and powerful cytotoxic drugs, also known as payloads. ADCs have direct therapeutic effects by targeting cancers with a strong payload. Another type of drug that uses antibodies are bsAbs, targeting two antigens by linking to antigen recognition sites or bridging cytotoxic immune cells to tumor cells, resulting in cancer immunotherapy. Three bsAbs and one ADC have been approved for use by the FDA and the EMA in 2022. Among these, two of the bsAbs and the one ADC are used for cancers. We introduced that bsADC, a combination of ADC and bsAbs, has yet to be approved and several candidates are in the early stages of clinical development in this review. bsADCs technology helps increase the specificity of ADCs or the internalization and killing ability of bsAbs. We also briefly discuss the application of click chemistry in the efficient development of ADCs and bsAbs as a conjugation strategy. The present review summarizes the ADCs, bsAbs, and bsADCs that have been approved for anti-cancer or currently in development. These strategies selectively deliver drugs to malignant tumor cells and can be used as therapeutic approaches for various types of cancer.

使用抗体药物偶联物(adc)和双特异性抗体(bsAbs)的工程方法旨在克服传统化疗和治疗性抗体的局限性,如耐药性和非特异性毒性。癌症免疫疗法已被证明是临床成功的检查点阻断和嵌合抗原受体T细胞治疗;然而,过度活跃的免疫系统仍然是一个主要问题。考虑到肿瘤环境的复杂性,针对两个或更多分子的策略将是有利的。我们强调针对癌症的多靶点平台策略的必要性和重要性。目前,约有400种adc和200多种bsab正在临床开发,用于几种适应症,具有良好的治疗活性迹象。adc包括识别肿瘤抗原的抗体,稳定连接药物的连接物,以及强大的细胞毒性药物,也被称为有效载荷。adc通过靶向具有强有效载荷的癌症具有直接的治疗作用。另一种使用抗体的药物是bsab,通过连接抗原识别位点或桥接细胞毒性免疫细胞与肿瘤细胞来靶向两种抗原,从而实现癌症免疫治疗。三种bsab和一种ADC已于2022年被FDA和EMA批准使用。其中,两种bsab和一种ADC用于癌症。我们在本综述中介绍了bsADC, ADC和bsab的组合,尚未获得批准,几个候选药物处于临床开发的早期阶段。bsADCs技术有助于提高adc的特异性或bsab的内化和杀伤能力。我们还简要讨论了点击化学作为一种共轭策略在adc和bsab的高效开发中的应用。本文综述了已获批或正在开发的adc、bsab和bsADCs。这些策略选择性地将药物输送到恶性肿瘤细胞,并可作为治疗各种类型癌症的方法。
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引用次数: 12
Naringin promotes fat browning mediated by UCP1 activation via the AMPK signaling pathway in 3T3-L1 adipocytes 柚皮苷通过AMPK信号通路促进3T3-L1脂肪细胞中UCP1激活介导的脂肪褐变
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-02-25 DOI: 10.1007/s12272-023-01432-7
Ho Seon Lee, Chan Uk Heo,  Young-Ho Song, Kyeong Lee, Chang-Ik Choi

Induction of the brown adipocyte-like phenotype in white adipocytes (fat browning) is considered a promising therapeutic strategy to treat obesity. Naringin, a citrus flavonoid, has antioxidant, anti-inflammatory, and anticancer activities. We examined the application of naringin as an anti-obesity compound based on an investigation of its induction of fat browning in 3T3-L1 adipocytes. Naringin did not induce lipid accumulation in differentiated 3T3-L1 adipocytes. Additionally, naringin reduced the expression levels of proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) involved in adipogenesis during lipid metabolism and increased the levels of PPARα and adiponectin involved in fatty acid oxidation. The expression levels of fat browning markers uncoupling protein 1 (UCP1; involved in thermogenesis) and PR domain containing 16 (PRDM16) increased. In addition, naringin treatment resulted in the activation of PPARγ coactivator 1-alpha (PGC-1α), a factor related to UCP1 transcription and mitochondrial biogenesis. Moreover, the expression of beige adipocyte-specific genes such as Cd137, Cited1, Tbx1, and Tmem26 was also induced. The small multi-lipid droplets characteristic of beige adipocytes indicated that naringin treatment increased the levels of all lipolysis markers (hormone-sensitive lipase [HSL], adipose triglyceride lipase [ATGL], perilipin [PLIN], and protein kinase A [PKA]). Adenosine monophosphate-activated protein kinase (AMPK) and UCP1 levels increased by treatment with naringin alone; this was possibly mediated by the stimulation of the AMPK signaling pathway. According to mechanistic studies, naringin activated the thermogenic protein UCP1 via the AMPK signaling pathway. In conclusion, naringin induces fat browning and is a promising therapeutic agent for metabolic disorders based on the regulation of lipid metabolism.

在白色脂肪细胞中诱导棕色脂肪细胞样表型(脂肪褐变)被认为是治疗肥胖的一种有前途的治疗策略。柚皮苷是一种柑橘类黄酮,具有抗氧化、抗炎和抗癌活性。我们在研究柚皮苷诱导3T3-L1脂肪细胞脂肪褐变的基础上,探讨了柚皮苷作为抗肥胖化合物的应用。柚皮苷不诱导分化的3T3-L1脂肪细胞的脂质积累。此外,柚皮素降低脂质代谢过程中参与脂肪形成的增殖因子激活受体γ (PPARγ)和CCAAT/增强子结合蛋白α (C/EBPα)的表达水平,增加参与脂肪酸氧化的PPARα和脂联素的水平。脂肪褐变标志物解偶联蛋白1 (UCP1;PR结构域16 (PRDM16)表达增加。此外,柚皮苷处理导致PPARγ共激活因子1- α (PGC-1α)的激活,这是一个与UCP1转录和线粒体生物发生相关的因子。此外,还诱导了米色脂肪细胞特异性基因Cd137、Cited1、Tbx1和Tmem26的表达。米色脂肪细胞的小多脂滴特征表明,柚皮苷处理增加了所有脂解标志物(激素敏感脂肪酶[HSL]、脂肪甘油三酯脂肪酶[ATGL]、佩里平[PLIN]和蛋白激酶A [PKA])的水平。单磷酸腺苷活化蛋白激酶(AMPK)和UCP1水平升高;这可能是通过刺激AMPK信号通路介导的。根据机制研究,柚皮苷通过AMPK信号通路激活产热蛋白UCP1。综上所述,柚皮苷可诱导脂肪褐变,是一种很有前景的基于脂质代谢调节的代谢紊乱药物。
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引用次数: 2
Dapagliflozin attenuates myocardial remodeling in hypertension by activating the circadian rhythm signaling pathway 达格列嗪通过激活昼夜节律信号通路来减轻高血压患者的心肌重塑。
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-02-02 DOI: 10.1007/s12272-023-01430-9
Jing Wang, Qiang She, Jianlin Du

Sodium-glucose cotransporter 2 inhibitor (SGLT2i) is a new kind of antidiabetic drug which has shown beneficial effects in reducing heart failure-related hospitalization and cardiovascular-related mortality. The mechanisms are complicated. Our study aimed to investigate the effects of dapagliflozin on the myocardium of spontaneously hypertensive rats (SHRs) without heart failure. Wistar-Kyoto rats were used as normal controls. SHRs were randomly divided into the SHR group and the -treated group. After 8 weeks of dapagliflozin treatment, the morphology of heart tissues was examined. The mRNA expression profiles were identified via RNA sequencing (RNA-Seq). Various analysis methods were used to find the differentially expressed genes (DEGs) to predict gene function and coexpression. After dapagliflozin treatment, systolic blood pressure was significantly reduced compared with that in the SHR group. Myocardial remodeling was ameliorated compared with that in the SHR group. After dapagliflozin intervention, 75 DEGs (|log2-fold change | > 0 and Q value < 0.05) were identified in the heart tissues compared to the SHR group. Quantitative real-time PCR analysis confirmed that the expression of the circadian rhythm genes Per3, Bhlhe41, and Nr1d1 was significantly upregulated, while the results were coincident with the RNA-Seq results. Dapagliflozin may effectively inhibit myocardial remodeling and regulate blood pressure. The mechanisms may be related to the activation of the circadian rhythm signaling pathway.

钠-葡萄糖协同转运蛋白2抑制剂(SGLT2i)是一种新型的抗糖尿病药物,在降低心力衰竭相关住院和心血管相关死亡率方面显示出有益的效果。机制是复杂的。本研究旨在研究达格列嗪对无心力衰竭的自发性高血压大鼠(SHR)心肌的影响。Wistar Kyoto大鼠作为正常对照。将SHR随机分为SHR组和治疗组。达格列嗪治疗8周后,检查心脏组织的形态学。通过RNA测序(RNA-Seq)鉴定mRNA表达谱。使用各种分析方法来寻找差异表达基因(DEGs),以预测基因功能和共表达。达格列嗪治疗后,收缩压与SHR组相比显著降低。与SHR组相比,心肌重构得到改善。达格列嗪干预后,75 DEG(|log2倍变化|>0和Q值
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引用次数: 3
Tumor lactic acid: a potential target for cancer therapy 肿瘤乳酸:癌症治疗的潜在靶点
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-02-02 DOI: 10.1007/s12272-023-01431-8
Jun-Kyu Byun

Tumor development is influenced by circulating metabolites and most tumors are exposed to substantially elevated levels of lactic acid and low levels of nutrients, such as glucose and glutamine. Tumor-derived lactic acid, the major circulating carbon metabolite, regulates energy metabolism and cancer cell signaling pathways, while also acting as an energy source and signaling molecule. Recent studies have yielded new insights into the pro-tumorigenic action of lactic acid and its metabolism. These insights suggest an anti-tumor therapeutic strategy targeting the oncometabolite lactic acid, with the aim of improving the efficacy and clinical safety of tumor metabolism inhibitors. This review describes the current understanding of the multifunctional roles of tumor lactic acid, as well as therapeutic approaches targeting lactic acid metabolism, including lactate dehydrogenase and monocarboxylate transporters, for anti-cancer therapy.

肿瘤的发展受到循环代谢产物的影响,大多数肿瘤都暴露在显著升高的乳酸水平和低水平的营养物质中,如葡萄糖和谷氨酰胺。肿瘤源性乳酸是主要的循环碳代谢产物,它调节能量代谢和癌症细胞信号通路,同时也是能量来源和信号分子。最近的研究对乳酸的促肿瘤作用及其代谢产生了新的见解。这些见解提出了一种靶向肿瘤代谢产物乳酸的抗肿瘤治疗策略,旨在提高肿瘤代谢抑制剂的疗效和临床安全性。这篇综述描述了目前对肿瘤乳酸多功能作用的理解,以及针对乳酸代谢的治疗方法,包括乳酸脱氢酶和单羧酸转运蛋白,用于抗癌治疗。
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引用次数: 2
Innate immune sensing of pathogens and its post-transcriptional regulations by RNA-binding proteins 病原体的先天免疫感知及其rna结合蛋白的转录后调控
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-02-01 DOI: 10.1007/s12272-023-01429-2
Ka Man Tse, Osamu Takeuchi

Innate immunity is one of the most ancient and conserved aspect of the immune system. It is responsible for an anti-infective response and has been intrinsically linked to the generation of inflammation. While the inflammatory response entails signaling to the adaptive immune system, it can be self-perpetuating and over-exaggerated, resulting in deleterious consequences, including cytokine storm, sepsis, and the development of inflammatory and autoimmune diseases. Cytokines are the defining features of the immune system. They are critical to mediation of inflammation and host immune defense, and are tightly regulated at several levels, including transcriptional and post-transcriptional levels. Recently, the role of post-transcriptional regulation in fine-tuning cytokine expression has become more appreciated. This interest has advanced our understanding of how various mechanisms are integrated and regulated to determine the amount of cytokine production in cells during inflammatory responses. Here, we would like to review how innate immunity recognizes and responds to pathogens by pattern-recognition receptors, and the molecular mechanisms regulating inflammatory responses, with a focus on the post-transcriptional regulations of inflammatory mediators by RNA-binding proteins, especially Regnase-1. Finally, we will discuss the regulatory mechanisms of Regnase-1 and highlight therapeutic strategies based on targeting Regnase-1 activity and its turnover as potential treatment options for chronic and autoimmune diseases.

先天免疫是免疫系统中最古老、最保守的方面之一。它负责抗感染反应,并与炎症的产生有着内在的联系。虽然炎症反应需要向适应性免疫系统发出信号,但它可能是自我延续和过度夸大的,导致有害的后果,包括细胞因子风暴、败血症、炎症和自身免疫性疾病的发展。细胞因子是免疫系统的决定性特征。它们对炎症和宿主免疫防御的介导至关重要,并在多个水平上受到严格调控,包括转录和转录后水平。近年来,转录后调控在细胞因子表达微调中的作用越来越受到重视。这种兴趣促进了我们对炎症反应期间细胞中细胞因子产生量的各种机制是如何整合和调节的理解。在这里,我们将回顾先天免疫如何通过模式识别受体识别和响应病原体,以及调节炎症反应的分子机制,重点关注rna结合蛋白,特别是Regnase-1对炎症介质的转录后调控。最后,我们将讨论Regnase-1的调控机制,并强调基于靶向Regnase-1活性及其周转的治疗策略,作为慢性和自身免疫性疾病的潜在治疗选择。
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引用次数: 2
Distinctive role of inflammation in tissue repair and regeneration 炎症在组织修复和再生中的独特作用
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-01-31 DOI: 10.1007/s12272-023-01428-3
Bokeum Choi, Changjun Lee, Je-Wook Yu

Inflammation is an essential host defense mechanism in response to microbial infection and tissue injury. In addition to its well-established role in infection, inflammation is actively involved in the repair of damaged tissues and restoration of homeostatic conditions after tissue injury. The intensity of the inflammatory response and types of cells involved in inflammation have a significant impact on the quality of tissue repair. Numerous immune cell subtypes participate in tissue repair and regeneration. In particular, immune cell-derived secretants, including cytokines and growth factors, can actively modulate the proliferation of resident stem cells or progenitor cells to facilitate tissue regeneration. These findings highlight the importance of inflammation during tissue repair and regeneration; however, the precise role of immune cells in tissue regeneration remains unclear. In this review, we summarize the current knowledge on the contribution of specific immune cell types to tissue repair and regeneration. We also discuss how inflammation affects the final outcome of tissue regeneration.

炎症是机体应对微生物感染和组织损伤的重要防御机制。除了在感染中的作用外,炎症还积极参与组织损伤后受损组织的修复和体内平衡状态的恢复。炎症反应的强度和参与炎症的细胞类型对组织修复的质量有重要影响。许多免疫细胞亚型参与组织修复和再生。特别是,免疫细胞源性分泌物,包括细胞因子和生长因子,可以主动调节常驻干细胞或祖细胞的增殖,促进组织再生。这些发现强调了炎症在组织修复和再生中的重要性;然而,免疫细胞在组织再生中的确切作用仍不清楚。在这篇综述中,我们总结了目前关于特定免疫细胞类型对组织修复和再生的贡献的知识。我们还讨论了炎症如何影响组织再生的最终结果。
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引用次数: 1
Isolation, structure elucidation, total synthesis, and biosynthesis of dermazolium A, an antibacterial imidazolium metabolite of a vaginal bacterium Dermabacter vaginalis 阴道皮杆菌抗菌咪唑代谢物dermazolium A的分离、结构解析、全合成和生物合成
IF 6.7 3区 医学 Q1 CHEMISTRY, MEDICINAL Pub Date : 2023-01-16 DOI: 10.1007/s12272-022-01424-z
Hye Ryeong Kim, Jonghwan Kim, Jae Sik Yu, Bum Soo Lee, Ki Hyun Kim, Chung Sub Kim

Dermabacter vaginalis is a human-derived bacterium isolated from vaginal fluid of a Korean female in 2016. Although several human-related species in Dermabacter genus have been reported there are few studies on their bioactive metabolites. Dermazolium A (1), a rare imidazolium metabolite, was isolated from D. vaginalis along with five known metabolites (2–6) and their chemical structures were determined by NMR, HRMS, and MS/MS data analysis. Feeding experiments using predicted precursors and biomimetic total synthesis of 1 corroborated its structure and led to suggestion of biosynthetic pathway of 1. Antibacterial tests on the isolated compounds showed that 1 is a mild antibacterial agent with MIC values of 41 µg/mL against methicillin-resistant Staphylococcus aureus (MRSA) USA300, Lacticaseibacillus paracasei subsp. paracasei KCTC 3510 and Brevibacterium epidermidis KCTC 3090.

阴道Dermabacter vaginalis是2016年从一名韩国女性阴道液中分离出的一种人类来源的细菌。尽管已经报道了几种Dermabacter属的人类亲缘物种,但对其生物活性代谢产物的研究很少。Dermazolium A(1)是一种罕见的咪唑代谢产物,与五种已知的代谢产物(2-6)一起从阴道D.vaginalis中分离出来,并通过NMR、HRMS和MS/MS数据分析确定了它们的化学结构。使用预测的前体和1的仿生全合成的饲养实验证实了其结构,并提出了1的生物合成途径。对分离化合物的抗菌试验表明,1是一种温和的抗菌剂,对耐甲氧西林金黄色葡萄球菌(MRSA)USA300、副干酪乳杆菌亚种的MIC值为41µg/mL。副酪蛋白KCTC 3510和表皮短杆菌KCTC 3090。
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引用次数: 5
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Archives of Pharmacal Research
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