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Development of a simple high-performance liquid chromatography-ultraviolet detection method for olaparib in patients with ovarian cancer. 卵巢癌患者奥拉帕尼的高效液相色谱-紫外检测方法的建立。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-12 Epub Date: 2023-12-03 DOI: 10.5582/ddt.2023.01074
Takeo Yasu, Ryosuke Nishijima, Risa Ikuta, Mikio Shirota, Haruko Iwase

Olaparib is a small-molecule inhibitor of poly(ADP)-ribose polymerase (PARP) used as maintenance therapy for recurrent ovarian cancer and newly diagnosed advanced ovarian cancer after initial chemotherapy. An exposure-toxicity correlation has been reported between the probability of anemia, a common adverse event associated with olaparib, and the steady-state minimum plasma concentration (Cmin) as well as the predicted maximum plasma concentration (Cmax). On the other hand, olaparib exhibits high interpatient variability with regard to the area under the concentration-time curve, Cmax, and Cmin. Therefore, we developed a simple and sensitive assay based on high-performance liquid chromatography with ultraviolet light (HPLC-UV) for the therapeutic drug monitoring of olaparib. The analysis was performed on an octadecylsilyl column with a mobile phase consisting of 0.5% KH2PO4 (pH 4.5) and acetonitrile (71:29, v/v), at a flow rate of 0.8 mL/min. Olaparib and an internal standard (imatinib) were well separated from the co-extracted material, with retention times of 13.6 and 11.5 min, respectively. The calibration curve for olaparib showed linearity over the concentration range of 0.10-10.0 μg/mL (r2 = 0.9998). The intra- and inter- day validation coefficients ranged from 1.79 to 4.13% and 1.37 to 3.55%, respectively. Measurement accuracy ranged from - 6.07 to 3.26%, with a recovery rate of more than 91.06%. The developed method was then applied to evaluate the plasma olaparib concentrations in patients with ovarian cancer. Our findings demonstrate that HPLC-UV is an economical, simple, and sensitive method for clinical application and holds promise for the effective drug monitoring of olaparib during ovarian cancer treatment.

奥拉帕尼(Olaparib)是一种小分子聚(ADP)-核糖聚合酶(PARP)抑制剂,用于卵巢癌复发和新诊断的晚期卵巢癌初始化疗后的维持治疗。有报道称,与奥拉帕尼相关的常见不良事件——贫血的概率与稳态最低血浆浓度(Cmin)以及预测最高血浆浓度(Cmax)之间存在暴露-毒性相关性。另一方面,奥拉帕尼在浓度-时间曲线下的面积、Cmax和Cmin方面表现出很高的患者间变异性。为此,建立了一种简便、灵敏的紫外高效液相色谱(HPLC-UV)检测奥拉帕尼治疗药物的方法。色谱柱为十八烷基硅基柱,流动相为0.5% KH2PO4 (pH 4.5)和乙腈(71:29,v/v),流速为0.8 mL/min。奥拉帕尼与内标(伊马替尼)分离较好,保留时间分别为13.6 min和11.5 min。奥拉帕尼在0.10 ~ 10.0 μg/mL范围内线性良好(r2 = 0.9998)。日内验证系数为1.79 ~ 4.13%,日内验证系数为1.37 ~ 3.55%。测定准确度为- 6.07 ~ 3.26%,回收率大于91.06%。然后应用该方法评价卵巢癌患者血浆奥拉帕尼浓度。本研究结果表明,高效液相色谱-紫外分光光度法是一种经济、简便、灵敏的临床应用方法,有望用于卵巢癌治疗期间奥拉帕尼的有效药物监测。
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引用次数: 0
Impact of anesthesia on postoperative breast cancer prognosis: A narrative review. 麻醉对癌症术后预后的影响:叙述性综述。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-12 Epub Date: 2023-10-31 DOI: 10.5582/ddt.2023.01065
Yi Tang, Shanshan Guo, Yao Chen, Li Liu, Minqiang Liu, Renliang He, Qiang Wu

The incidence of breast cancer has exhibited an annually increasing trend, and the disease has become the most common malignant tumour worldwide. Currently, the primary treatment for breast cancer is surgical resection. However, metastatic recurrence is the main cause of cancer-related death in this patient population. Various factors are associated with breast cancer prognosis, and anaesthesia-induced changes in the tumour microenvironment have attracted increasing attention. To date, however, it remains unclear whether anaesthetic drugs have a positive or negative impact on cancer outcomes after surgery. The present article reviews the effects of different anaesthetics on the postoperative prognosis of breast cancer surgery to guide the choice of anaesthetic technique(s) and agents for such patients.

癌症的发病率呈逐年上升趋势,已成为世界范围内最常见的恶性肿瘤。目前,癌症的主要治疗方法是手术切除。然而,转移性复发是该患者群体中癌症相关死亡的主要原因。多种因素与乳腺癌症预后相关,麻醉学诱导的肿瘤微环境变化引起了越来越多的关注。然而,到目前为止,麻醉药物对癌症手术后的结果是积极影响还是消极影响仍不清楚。本文综述了不同麻醉剂对癌症手术后预后的影响,以指导此类患者麻醉技术和药物的选择。
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引用次数: 0
Quercetin antagonized advanced glycated end products induced apoptosis and functional inhibition of fibroblasts from the prolapsed uterosacral ligament. 槲皮素拮抗晚期糖基化终产物诱导子宫骶韧带脱垂成纤维细胞凋亡和功能抑制。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-12 Epub Date: 2023-12-03 DOI: 10.5582/ddt.2023.01047
Yizhen Sima, Junwei Li, Leimei Xu, Chengzhen Xiao, Lisha Li, Ling Wang, Yisong Chen

The altered behaviors and functions of pelvic floor fibroblasts are pathophysiological changes of pelvic organ prolapse (POP). Our previous study showed that advanced glycated end products (AGEs) accumulated in the pelvic tissues of POP and induced fibroblast apoptosis. The study was designed to investigate whether quercetin antagonize AGEs-induced apoptosis and functional inhibition of fibroblasts. The uptake of 5-ethynyl-2'-deoxyuridine (EdU) was evaluated for cell proliferation. Flow cytometric analysis was applied for cell apoptosis. Intracellular reactive oxygen species (ROS) content was determined by the fluorescence of dichlorofluorescein (DCF). The contractility of fibroblasts was measured by collagen gel contraction assay. The expressions of extracellular matrix (ECM) related genes and the expression of miR-4429 and caspase-3 were quantified by qPCR. The expressions of phosphatase and tensin homolog (PTEN), phosphoinositide 3-kinase (PI3K), serine-threonine kinase (Akt), and phosphorylated Akt (p-Akt) were analyzed by Western Blot. The down-regulation of miR-4429 was achieved by cell transfection. Quercetin antagonized AGEs-induced apoptosis, proliferation inhibition, and ROS increase in fibroblasts. Quercetin did not alleviate AGEs-induced contractile impairment of fibroblasts. Quercetin reduced the gene expressions of lysyl oxidase like protein 1 (LOXL1)and matrix metallopeptidase 1 (MMP1), and increased the gene expressions of lysyl oxidase (LOX) and fibrillin 2 (FBN2) in fibroblasts. Quercetin reversed AGEs-induced upregulation of PTEN and downregulation of PI3K, P-Akt, and miR-4429 in fibroblasts. The inhibitory effect of quercetin on AGEs-induced fibroblast apoptosis was inhibited by downregulating the expression of miR-4429. In conclusion, quercetin antagonized AGEs-induced apoptosis and functional inhibition of fibroblasts from the prolapsed uterosacral ligament. And inhibiting AGEs-induced down-regulation of miR-4429/PTEN/PI3K/Akt pathway was the mechanism underlying the antagonistic effect of quercetin on AGEs-induced apoptosis.

盆底成纤维细胞行为和功能的改变是盆腔器官脱垂(POP)的病理生理改变。我们之前的研究表明,晚期糖基化终产物(AGEs)在POP的盆腔组织中积累并诱导成纤维细胞凋亡。研究槲皮素对衰老诱导的成纤维细胞凋亡和功能抑制的拮抗作用。评估5-乙基-2'-脱氧尿苷(EdU)的摄取对细胞增殖的影响。流式细胞术检测细胞凋亡。采用二氯荧光素(DCF)荧光法测定细胞内活性氧(ROS)含量。采用胶原凝胶收缩法测定成纤维细胞的收缩能力。采用qPCR定量检测细胞外基质(extracellular matrix, ECM)相关基因的表达以及miR-4429、caspase-3的表达。Western Blot法分析磷酸酶及紧张素同源物(PTEN)、磷酸肌肽3-激酶(PI3K)、丝氨酸-苏氨酸激酶(Akt)、磷酸化Akt (p-Akt)的表达。通过细胞转染实现miR-4429的下调。槲皮素可拮抗ages诱导的成纤维细胞凋亡、增殖抑制和ROS增加。槲皮素不能减轻ages诱导的成纤维细胞收缩损伤。槲皮素降低了成纤维细胞中赖氨酸氧化酶样蛋白1 (LOXL1)和基质金属肽酶1 (MMP1)的基因表达,增加了赖氨酸氧化酶(LOX)和纤维蛋白2 (FBN2)的基因表达。槲皮素逆转了ages诱导的成纤维细胞中PTEN的上调和PI3K、P-Akt和miR-4429的下调。槲皮素通过下调miR-4429的表达抑制ages诱导的成纤维细胞凋亡。槲皮素可拮抗ages诱导的子宫骶韧带脱垂成纤维细胞凋亡和功能抑制。槲皮素抑制衰老诱导的miR-4429/PTEN/PI3K/Akt通路下调是槲皮素抑制衰老诱导的细胞凋亡的机制。
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引用次数: 0
Which biomarkers predict hard-to-heal diabetic foot ulcers? A scoping review. 哪些生物标志物可预测难以愈合的糖尿病足溃疡?范围综述。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-12 Epub Date: 2023-12-22 DOI: 10.5582/ddt.2023.01086
Qi Qin, Daijiro Haba, Gojiro Nakagami

Diabetic foot ulcers (DFUs) often develop into hard-to-heal wounds due to complex factors. Several biomarkers capable of identifying those at risk of delayed wound healing have been reported. Controlling or targeting these biomarkers could prevent the progression of DFUs into hard-to-heal wounds. This scoping review aimed to identify the key biomarkers that can predict hard-to-heal DFUs. Studies that reported biomarkers related to hard-to-heal DFUs, from 1980 to 2023, were mapped. Studies were collected from the following databases: MEDLINE, CINAHL, EMBASE, and ICHUSHI (Japana Centra Revuo Medicina), search terms included "diabetic," "ulcer," "non-healing," and "biomarker." A total of 808 articles were mapped, and 14 (10 human and 4 animal studies) were included in this review. The ulcer characteristics in the clinical studies varied. Most studies focused on either infected wounds or neuropathic wounds, and patients with ischemia were usually excluded. Among the reported biomarkers for the prediction of hard-to-heal DFUs, the pro-inflammatory cytokine CXCL-6 in wound fluid from non-infected and non-ischemic wounds had the highest prediction accuracy (area under the curve: 0.965; sensitivity: 87.27%; specificity: 95.56%). CXCL-6 levels could be a useful predictive biomarker for hard-to-heal DFUs. However, CXCL6, a chemoattractant for neutrophilic granulocytes, elicits its chemotactic effects by combining with the chemokine receptors CXCR1 and CXCR2, and is involved in several diseases. Therefore, it's difficult to use CXCL6 as a prevention or treatment target. Targetable specific biomarkers for hard-to-heal DFUs need to be determined.

糖尿病足溃疡(DFU)通常会因复杂的因素发展成为难以愈合的伤口。据报道,有几种生物标志物能够识别伤口延迟愈合的高危人群。控制或靶向这些生物标志物可以防止 DFU 发展成为难以愈合的伤口。本次范围界定综述旨在确定可预测 DFU 难以愈合的关键生物标志物。我们对 1980 年至 2023 年期间报告了与难以愈合的 DFU 相关的生物标志物的研究进行了映射。研究资料来自以下数据库:MEDLINE、CINAHL、EMBASE 和 ICHUSHI(Japana Centra Revuo Medicina),检索词包括 "糖尿病"、"溃疡"、"不愈合 "和 "生物标志物"。共检索到 808 篇文章,其中 14 篇(10 篇人体研究和 4 篇动物研究)被纳入本综述。临床研究中的溃疡特征各不相同。大多数研究侧重于感染性伤口或神经性伤口,缺血患者通常被排除在外。在已报道的预测 DFU 难以愈合的生物标志物中,非感染和非缺血伤口的伤口液中的促炎细胞因子 CXCL-6 预测准确率最高(曲线下面积:0.965;灵敏度:87.27%;特异性:95.56%)。CXCL-6水平可以作为难以愈合的DFU的有效预测生物标志物。然而,CXCL6 是中性粒细胞的趋化吸引剂,通过与趋化因子受体 CXCR1 和 CXCR2 结合产生趋化作用,并与多种疾病有关。因此,很难将 CXCL6 作为预防或治疗目标。需要确定难以愈合的 DFU 的可靶向特异性生物标志物。
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引用次数: 0
Polycystic ovary syndrome and adverse pregnancy outcomes: potential role of decidual function. 多囊卵巢综合征与不良妊娠结局:蜕膜功能的潜在作用。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-12 Epub Date: 2023-12-27 DOI: 10.5582/ddt.2023.01096
Lisha Li, Hanting Ge, Jing Zhou, Jing Wang, Ling Wang

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting fertility and mental health among women of reproductive age. In addition to anovulation and hyperandrogenism, patients also experience metabolic issues, such as insulin resistance, obesity, and dyslipidemia, as well as chronic low-grade inflammation throughout the body. Recent studies have shown that even with assisted reproductive technology to treat anovulatory issues, patients with PCOS still have higher rates of adverse pregnancy outcomes and abortion compared to normal pregnancies. These findings suggest that PCOS may impair the endometrium and disrupt the onset and maintenance of healthy pregnancies. Decidualization is a crucial step in the process of healthy pregnancy, during which endometrial stromal cells (ESCs) differentiate into secretory decidual stromal cells (DSCs) regulated by hormones and local metabolism. This article comprehensively reviews the pathological processes of PCOS and the mechanisms involved in its impaired decidualization. In addition, we explore how PCOS increases the incidence of adverse pregnancy outcomes (APO). By gaining a better understanding of the adverse effects of PCOS on pregnancy and its specific mechanisms, we hope to provide a theoretical basis for reducing APO and improving the live birth rate among women with PCOS.

多囊卵巢综合征(PCOS)是一种常见的内分泌疾病,影响育龄妇女的生育能力和心理健康。除了无排卵和雄激素过多外,患者还会出现新陈代谢问题,如胰岛素抵抗、肥胖和血脂异常,以及全身慢性低度炎症。最近的研究表明,即使采用辅助生殖技术治疗无排卵问题,多囊卵巢综合症患者的不良妊娠结局和流产率仍高于正常妊娠。这些研究结果表明,多囊卵巢综合症可能会损害子宫内膜,干扰健康妊娠的发生和维持。蜕膜化是健康妊娠过程中的一个关键步骤,在这一过程中,子宫内膜基质细胞(ESCs)在激素和局部代谢的调节下分化成分泌型蜕膜基质细胞(DSCs)。本文全面回顾了多囊卵巢综合征的病理过程及其蜕膜化受损的相关机制。此外,我们还探讨了多囊卵巢综合征如何增加不良妊娠结局(APO)的发生率。通过更好地了解多囊卵巢综合症对妊娠的不良影响及其具体机制,我们希望为减少多囊卵巢综合症妇女的不良妊娠结局和提高活产率提供理论依据。
{"title":"Polycystic ovary syndrome and adverse pregnancy outcomes: potential role of decidual function.","authors":"Lisha Li, Hanting Ge, Jing Zhou, Jing Wang, Ling Wang","doi":"10.5582/ddt.2023.01096","DOIUrl":"10.5582/ddt.2023.01096","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting fertility and mental health among women of reproductive age. In addition to anovulation and hyperandrogenism, patients also experience metabolic issues, such as insulin resistance, obesity, and dyslipidemia, as well as chronic low-grade inflammation throughout the body. Recent studies have shown that even with assisted reproductive technology to treat anovulatory issues, patients with PCOS still have higher rates of adverse pregnancy outcomes and abortion compared to normal pregnancies. These findings suggest that PCOS may impair the endometrium and disrupt the onset and maintenance of healthy pregnancies. Decidualization is a crucial step in the process of healthy pregnancy, during which endometrial stromal cells (ESCs) differentiate into secretory decidual stromal cells (DSCs) regulated by hormones and local metabolism. This article comprehensively reviews the pathological processes of PCOS and the mechanisms involved in its impaired decidualization. In addition, we explore how PCOS increases the incidence of adverse pregnancy outcomes (APO). By gaining a better understanding of the adverse effects of PCOS on pregnancy and its specific mechanisms, we hope to provide a theoretical basis for reducing APO and improving the live birth rate among women with PCOS.</p>","PeriodicalId":47494,"journal":{"name":"Drug Discoveries and Therapeutics","volume":" ","pages":"378-388"},"PeriodicalIF":3.1,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139040742","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: 0
Anti-senescence effects of 4-methoxychalcone and 4-bromo-4'-methoxychalcone on human endothelial cells. 4-甲氧基查尔酮和 4-溴-4'-甲氧基查尔酮对人类内皮细胞的抗衰老作用
IF 1.9 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 DOI: 10.5582/ddt.2024.01034
Xin-Yi Tien, Yean Kee Lee, Pooi-Fong Wong, Yi-Sheng Khor, Dharmani Devi Murugan, Iskandar Abdullah

Senolytics are drugs that specifically target senescent cells. Flavonoids such as quercetin and fisetin possess selective senolytic activities. This study aims to investigate if chalcones exhibit anti-senescence activities. Anti-senescence effect of 11 chalcone derivatives on the replicative senescence human aortic endothelial cells (HAEC) and human fetal lung fibroblasts (IMR90) was evaluated. Compound 2 (4-methoxychalcone) and compound 4 (4-bromo-4'-methoxychalcone) demonstrated increased cytotoxicity in senescent HAEC compared to young HAEC, with significant differences on IC50 values. Their anti-senescence effects on HAEC exceeded fisetin. Higher selectivity of compound 4 toward HAEC over IMR90 could be attributed to 4-methoxy (4-OMe) substitution at ring A (R1). Chalcone derivatives have potentials as senolytics in mitigating replicative senescence, warranting further research and development on chalcones as anti-senescent agent.

衰老药是专门针对衰老细胞的药物。槲皮素和鱼黄素等黄酮类化合物具有选择性的衰老分解活性。本研究旨在探讨查尔酮是否具有抗衰老活性。研究评估了 11 种查尔酮衍生物对复制衰老的人主动脉内皮细胞(HAEC)和人胎肺成纤维细胞(IMR90)的抗衰老作用。与年轻的 HAEC 相比,化合物 2(4-甲氧基查尔酮)和化合物 4(4-溴-4'-甲氧基查尔酮)在衰老的 HAEC 中显示出更强的细胞毒性,且 IC50 值存在显著差异。它们对 HAEC 的抗衰老作用超过了鱼藤酮。与 IMR90 相比,化合物 4 对 HAEC 更高的选择性可归因于 A 环(R1)上的 4-甲氧基(4-OMe)取代。查耳酮衍生物在缓解复制衰老方面具有潜在的分解作用,因此有必要进一步研究和开发查耳酮类抗衰老剂。
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引用次数: 0
The S-Nitrosylation of Septin2 (SNO-Septin2) axis: A novel potential therapeutic target for treating aneurysms and dissection. Septin2的S-亚硝基化(SNO-Septin2)轴:治疗动脉瘤和夹层的潜在新靶点
IF 1.9 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2024-01-01 DOI: 10.5582/ddt.2024.01047
Ying Zhang, Hongtao Qu, Chuanhua Li, Lanfang Li, Lu He

Aortic aneurysm and aortic dissection (AAD) are severe life-threatening cardiovascular disorders for which no approved pharmaceutical therapies are currently available. Protein S-nitrosylation (SNO) is a typical redox-dependent posttranslational modification whose role in AAD has yet to be described. Recently, Zhang et al. revealed for the first time that SNO modification of macrophage cytoskeletal protein septin2 promotes vascular inflammation and extracellular matrix degradation in aortic aneurysm. Mechanically, the TIAM1-RAC1(T lymphoma invasion and metastasis-inducing protein 1-Ras-related C3 botulinum toxin substrate 1) axis participates in the progression of AAD induced with S-nitrosylated septin2. More importantly, developing R-ketorolac and NSC23766 compounds that specifically target the TIAM1-RAC1 pathway may be new a potential strategy for alleviating AAD.

主动脉瘤和主动脉夹层(AAD)是严重威胁生命的心血管疾病,目前还没有获得批准的药物疗法。蛋白质 S-亚硝基化(SNO)是一种典型的氧化还原依赖性翻译后修饰,其在 AAD 中的作用尚未被描述。最近,Zhang 等人首次揭示了巨噬细胞细胞骨架蛋白 septin2 的 SNO 修饰会促进主动脉瘤中的血管炎症和细胞外基质降解。从机理上讲,TIAM1-RAC1(T淋巴瘤侵袭和转移诱导蛋白1-Ras相关C3肉毒毒素底物1)轴参与了S-亚硝基化septin2诱导的AAD进展。更重要的是,开发特异性靶向 TIAM1-RAC1 通路的 R-Ketorolac 和 NSC23766 化合物可能是缓解 AAD 的一种新策略。
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引用次数: 0
Complete trisomy 9 detected by noninvasive prenatal testing and confirmed by amniocentesis. 通过无创产前检测检测到的完全性9号三体,并通过羊水穿刺证实。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2023-11-18 Epub Date: 2023-10-11 DOI: 10.5582/ddt.2023.01051
Feixiang Huang, Jing Zhou, Zheyun Xu, Qing Qi, Hongmei Sun, Lei Chen, Ling Wang

Complete chromosome 9 trisomy (T9) is a rare and fatal chromosomal disorder. We performed non-invasive prenatal testing (NIPT) in a patient with threatened abortion symptoms and found that the fetal was at risk for complete chromosome 9 trisomy. This shows that NIPT has certain accuracy in detecting trisomy of chromosome 9, which provide options for prenatal diagnosis of rare chromosomal abnormalities.

完全性9号染色体三体(T9)是一种罕见且致命的染色体疾病。我们对一名有先兆流产症状的患者进行了无创产前检测(NIPT),发现胎儿有完全9号染色体三体的风险。这表明NIPT在检测9号染色体三体性方面具有一定的准确性,为罕见染色体异常的产前诊断提供了选择。
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引用次数: 0
Hypofibrinolytic phenotype in Tsumura Suzuki Obese Diabetes (TSOD) mice unrelated to hyperglycemia. Tsumura Suzuki肥胖糖尿病(TSOD)小鼠的纤溶功能低下表型与高血糖无关。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2023-11-18 Epub Date: 2023-10-14 DOI: 10.5582/ddt.2023.01064
Naoki Ohkura, Riyo Morimoto-Kamata, Yuichi Kamikubo, Yoshihisa Takahashi, Katsutaka Oishi

Obesity and diabetes mellitus are associated with increased risk of arterial thrombosis and venous thromboembolism. Tsumura Suzuki Obese Diabetes (TSOD) mice are useful models for elucidating the molecular mechanisms of these diseases. We investigated normoglycemic [Ng]-TSOD mice with a metabolic abnormality that was accompanied by a coagulative and fibrinolytic state with a phenotype that distinctly differed from that of standard TSOD mice. As in TSOD mice, plasminogen activation inhibitor-1 (PAI-1) that inhibits fibrinolysis was substantially augmented in Ng-TSOD mice, suggesting that they are hypofibrinolytic. However, blood clotting parameters were within the normal range in Ng-TSOD mice. These findings indicated that Ng-TSOD mice are novel models with a hypofibrinolytic phenotype that is not associated with hyperglycemia.

肥胖和糖尿病与动脉血栓形成和静脉血栓栓塞的风险增加有关。Tsumura Suzuki肥胖糖尿病(TSOD)小鼠是阐明这些疾病的分子机制的有用模型。我们研究了血糖正常的[Ng]-TSOD小鼠,其代谢异常伴有凝血和纤溶状态,其表型与标准TSOD小鼠明显不同。与TSOD小鼠一样,抑制纤维蛋白溶解的纤溶酶原激活抑制剂-1(PAI-1)在Ng TSOD小鼠中显著增强,表明它们是低纤溶性的。然而,Ng-TSOD小鼠的凝血参数在正常范围内。这些发现表明,Ng-TSOD小鼠是具有与高血糖无关的低纤溶表型的新型模型。
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引用次数: 0
FASN promotes gallbladder cancer progression and reduces cancer cell sensitivity to gemcitabine through PI3K/AKT signaling. FASN通过PI3K/AKT信号促进胆囊癌症进展并降低癌症细胞对吉西他滨的敏感性。
IF 3.1 Q3 PHARMACOLOGY & PHARMACY Pub Date : 2023-11-18 Epub Date: 2023-09-22 DOI: 10.5582/ddt.2023.01036
Haihong Cheng, Yuxin Sun, Xiaopeng Yu, Di Zhou, Jun Ding, Shouhua Wang, Fei Ma

Lipid metabolism plays an important role in the growth and development of tumors. However, the role of lipid metabolism in gallbladder cancer (GBC) has not been clearly clarified. Here, we demonstrated that fatty acid synthase (FASN), a key enzyme in de novo fatty acid biosynthesis, had upregulated expression in GBC samples both at protein and mRNA levels. Analysis of clinical data indicated the association between elevated FASN expression and poorer histology grades. Furthermore, FASN activity impairment through FASN knockdown or treatment with orlistat resulted in the inhibition of cell proliferation and migration, as well as increased sensitivity to gemcitabine. Both FASN knockdown and orlistat treatment induced cell apoptosis. Mechanistically, impairment of FASN activity suppressed the activation of the PI3K/AKT signaling pathway, which led to increased cell apoptosis and sensitivity to gemcitabine. These findings were also validated through nude mouse xenograft models, thus highlighting the potential of targeting FASN as a clinical treatment strategy. Collectively, the present study underscores the crucial role of FASN in the progression of gallbladder cancer via the PI3K/AKT pathway.

脂质代谢在肿瘤的生长发育中起着重要作用。然而,脂质代谢在胆囊癌症(GBC)中的作用尚未明确。在这里,我们证明了脂肪酸合成酶(FASN),一种新脂肪酸生物合成的关键酶,在GBC样品中的蛋白质和mRNA水平上都上调了表达。临床数据分析表明FASN表达升高与组织学分级较差之间存在关联。此外,通过FASN敲除或用奥利司他治疗引起的FASN活性损伤导致细胞增殖和迁移的抑制,以及对吉西他滨的敏感性增加。FASN敲除和奥利司他治疗均诱导细胞凋亡。从机制上讲,FASN活性的损伤抑制了PI3K/AKT信号通路的激活,从而导致细胞凋亡和对吉西他滨的敏感性增加。这些发现也通过裸鼠异种移植物模型得到了验证,从而突出了靶向FASN作为临床治疗策略的潜力。总之,本研究强调了FASN通过PI3K/AKT途径在胆囊癌症进展中的关键作用。
{"title":"FASN promotes gallbladder cancer progression and reduces cancer cell sensitivity to gemcitabine through PI3K/AKT signaling.","authors":"Haihong Cheng, Yuxin Sun, Xiaopeng Yu, Di Zhou, Jun Ding, Shouhua Wang, Fei Ma","doi":"10.5582/ddt.2023.01036","DOIUrl":"10.5582/ddt.2023.01036","url":null,"abstract":"<p><p>Lipid metabolism plays an important role in the growth and development of tumors. However, the role of lipid metabolism in gallbladder cancer (GBC) has not been clearly clarified. Here, we demonstrated that fatty acid synthase (FASN), a key enzyme in de novo fatty acid biosynthesis, had upregulated expression in GBC samples both at protein and mRNA levels. Analysis of clinical data indicated the association between elevated FASN expression and poorer histology grades. Furthermore, FASN activity impairment through FASN knockdown or treatment with orlistat resulted in the inhibition of cell proliferation and migration, as well as increased sensitivity to gemcitabine. Both FASN knockdown and orlistat treatment induced cell apoptosis. Mechanistically, impairment of FASN activity suppressed the activation of the PI3K/AKT signaling pathway, which led to increased cell apoptosis and sensitivity to gemcitabine. These findings were also validated through nude mouse xenograft models, thus highlighting the potential of targeting FASN as a clinical treatment strategy. Collectively, the present study underscores the crucial role of FASN in the progression of gallbladder cancer via the PI3K/AKT pathway.</p>","PeriodicalId":47494,"journal":{"name":"Drug Discoveries and Therapeutics","volume":" ","pages":"328-339"},"PeriodicalIF":3.1,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41139629","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: 0
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