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Anticancer Properties of Baicalin against Breast Cancer and other Gynecological Cancers: Therapeutic Opportunities based on Underlying Mechanisms. 黄芩苷对乳腺癌和其他妇科癌症的抗癌特性:基于基本机制的治疗机会。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429263063231204095516
Mohammad Hossein Pourhanifeh, Hossein Farrokhi-Kebria, Parsa Mostanadi, Tahereh Farkhondeh, Saeed Samarghandian

Gynecological cancers are serious life-threatening diseases responsible for high morbidity and mortality around the world. Chemotherapy, radiotherapy, and surgery are considered standard therapeutic modalities for these cancers. Since the mentioned treatments have undesirable side effects and are not effective enough, further attempts are required to explore potent complementary and/or alternative treatments. This study was designed to review and discuss the anticancer potentials of baicalin against gynecological cancers based on causal mechanisms and underlying pathways. Traditional medicine has been used for thousands of years in the therapy of diverse human diseases. The therapeutic effects of natural compounds like baicalin have been widely investigated in cancer therapy. Baicalin was effective against gynecological cancers by regulating key cellular mechanisms, including apoptosis, autophagy, and angiogenesis. Baicalin exerted its anticancer property by regulating most molecular signaling pathways, including PI3K/Akt/mTOR, NFκB, MAPK/ERK, and Wnt/β-catenin. However, more numerous experimental and clinical studies should be designed to find the efficacy of baicalin and the related mechanisms of action.

妇科癌症是严重威胁生命的疾病,在全世界都有很高的发病率和死亡率。化疗、放疗和手术被认为是治疗这些癌症的标准方法。由于上述治疗方法存在不良副作用且不够有效,因此需要进一步尝试探索有效的补充和/或替代治疗方法。本研究旨在根据黄芩苷的成因机制和潜在途径,回顾和讨论黄芩苷对妇科癌症的抗癌潜力。几千年来,传统医学一直被用于治疗人类的各种疾病。黄芩苷等天然化合物在癌症治疗中的疗效已得到广泛研究。黄芩苷通过调节关键的细胞机制,包括细胞凋亡、自噬和血管生成,对妇科癌症有效。黄芩苷通过调节大多数分子信号通路(包括 PI3K/Akt/mTOR、NFκB、MAPK/ERK 和 Wnt/β-catenin)发挥抗癌作用。然而,要找到黄芩苷的功效和相关作用机制,还需要进行更多的实验和临床研究。
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引用次数: 0
Mechanism, Potential, and Concerns of Immunotherapy for Hepatocellular Carcinoma and Liver Transplantation. 肝细胞癌和肝移植免疫疗法的机理、潜力和担忧。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429310703240823045808
Bruno Sensi, Roberta Angelico, Luca Toti, Luigi Conte, Alessandro Coppola, Giuseppe Tisone, Tommaso Maria Manzia

In the last decade, immunotherapy (IT) has revolutionized oncology and found indications in many cancers, including hepatocellular carcinoma (HCC). In HCC, IT has become the leading systemic therapy for advanced diseases. At the same time, it carries the promise of being a valuable therapy in other settings, including intermediate-stage and unresectable disease, as a downstaging or conversion modality. More controversial is the role of IT in relationship to liver transplantation (LT): on one side, it could be a helpful tool to control or downstage HCC before LT or to treat tumor recurrence after LT, while on the other, it carries the risk of graft rejection and graft loss. This review aims to cover these concerns in depth and unravel the current literature.

近十年来,免疫疗法(IT)在肿瘤学领域掀起了一场革命,并在包括肝细胞癌(HCC)在内的多种癌症中找到了适应症。在肝细胞癌领域,免疫疗法已成为治疗晚期疾病的主要系统疗法。与此同时,在其他情况下,包括中晚期和无法切除的疾病,它也有望成为一种有价值的疗法,作为一种降期或转换模式。更具争议性的是 IT 在肝移植(LT)中的作用:一方面,它可能是在 LT 前控制或降低 HCC 分期或在 LT 后治疗肿瘤复发的有用工具,而另一方面,它又存在移植物排斥和移植物丢失的风险。本综述旨在深入探讨这些问题,并对现有文献进行解读。
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引用次数: 0
The Roles of mTOR Signaling in Nasopharyngeal Carcinoma: From Pathogenesis to Therapy mTOR信号在鼻咽癌中的作用:从发病机制到治疗
Pub Date : 2024-01-01 DOI: 10.2174/0118761429293675240709061332
Ting Gong, Gui Cao, Danyang Sun, Tongtong Ge, Ping Li

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy caused by cancer of the mucosal epithelial cells of the nasopharynx. Most patients with NPC present with distant metastases and treatment resistance, both of which challenge current anti-tumour drugs. The mammalian target of the rapamycin (mTOR) signalling pathway is one of the most highly activated signalling pathways in NPC and plays an important role in various cellular activities. Dysfunction of mTOR and related signalling pathways induces tumour metabolism and growth. In this review, we summarize current evidence to evaluate the potential mechanisms by which mTOR is implicated in NPC. It was found that activating mTOR and its upstream and downstream signalling can promote tumor growth and survival of NPC. It is possible that EMT and autophagy regulated by cellular mTOR signalling activities may be implicated in the metastases and radioresistance of NPC.

鼻咽癌是一种由鼻咽粘膜上皮细胞癌变引起的上皮性恶性肿瘤。大多数鼻咽癌患者都有远处转移和耐药性,这两种情况都对目前的抗肿瘤药物提出了挑战。哺乳动物雷帕霉素靶标(mTOR)信号通路是鼻咽癌中最活跃的信号通路之一,在各种细胞活动中发挥着重要作用。mTOR及相关信号通路的功能障碍会诱导肿瘤的代谢和生长。在本综述中,我们总结了目前的证据,以评估 mTOR 与鼻咽癌相关的潜在机制。研究发现,激活 mTOR 及其上下游信号可促进鼻咽癌的肿瘤生长和存活。由细胞mTOR信号活动调控的EMT和自噬可能与鼻咽癌的转移和放射抗性有关。
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引用次数: 0
Effect of Chrysin and Chrysin Nanocrystals on Chlorpyrifos-Induced Dysfunction of the Hypothalamic-Pituitary-Testicular Axis in Rats 蛹虫草素和蛹虫草素纳米晶体对毒死蜱诱导的大鼠下丘脑-垂体-睾丸轴功能障碍的影响
Pub Date : 2024-01-01 DOI: 10.2174/0118761429305457240826093330
Tahereh Farkhondeh, Babak Roshanravan, Fariborz Samini, Saeed Samarghandian

Aims and background: The escalating global concerns regarding reproductive health underscore the urgency of investigating the impact of environmental pollutants on fertility. This study aims to focus on Chlorpyrifos (CPF), a widely-used organophosphate insecticide, and explores its adverse influence on the hypothalamic-pituitary-testicular axis in Wistar male rats. This study explores the potential protective effects of chrysin nanocrystal (CHN), a flavonoid with known antioxidant and anti-inflammatory properties, against CPF-induced impairments in male Wistar rats.

Methods: Chrysin nanocrystals were prepared using a solvent precipitation method. Six sets of male Wistar rats were subjected to 30 days of treatment, comprising a control group, a group treated solely with CPF, groups treated with CHN at doses of 5 mg/kg and 10 mg/kg, and groups co-treated with CPF and CHN. Serum levels of reproductive hormones, enzyme biomarkers of testicular function, oxidative stress, and inflammatory biomarkers were assessed. Additionally, histological examinations were conducted on the hypothalamus, testes, and epididymis.

Results: CHN exhibited antioxidant and anti-inflammatory properties, effectively counteracting CPF-induced reductions in Luteinizing Hormone (LH), serum testosterone, Follicle-Stimulating Hormone (FSH), and testicular enzyme biomarkers. Moreover, CHN enhanced antioxidant defenses, as evidenced by decreased malondialdehyde (MDA) and increased glutathione (GSH) levels in the hypothalamus, and testes, epididymis. Inflammatory markers, including nitric oxide (NO), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), were significantly reduced in CHN co-treated groups compared to the CPF-only group. Histopathological analyses confirmed the protective effects of CHN on tissue integrity.

Conclusion: Chrysin nanocrystal demonstrated promising potential in mitigating CPF-induced reproductive deficits in male rats through its anti-inflammatory and antioxidant properties. This study provides valuable insights into therapeutic interventions against environmental toxin-induced reproductive toxicity, emphasizing the potential of chrysin nanocrystals as a protective agent in the context of CPF exposure.

目的和背景:全球对生殖健康的关注不断升级,这凸显了调查环境污染物对生育能力影响的紧迫性。本研究旨在关注一种广泛使用的有机磷杀虫剂--毒死蜱(CPF),并探讨其对 Wistar 雄性大鼠下丘脑-垂体-睾丸轴的不利影响。本研究探讨了菊黄素纳米晶体(CHN)的潜在保护作用,菊黄素纳米晶体是一种具有已知抗氧化和抗炎特性的类黄酮,可防止氯化石蜡诱导的雄性 Wistar 大鼠下丘脑-垂体-睾丸轴损伤:方法:采用溶剂沉淀法制备金黄素纳米晶体。对六组雄性 Wistar 大鼠进行为期 30 天的治疗,包括对照组、仅用氯化石蜡治疗组、用 CHN(剂量分别为 5 毫克/千克和 10 毫克/千克)治疗组以及用氯化石蜡和 CHN 联合治疗组。对血清中的生殖激素水平、睾丸功能酶生物标志物、氧化应激和炎症生物标志物进行了评估。此外,还对下丘脑、睾丸和附睾进行了组织学检查:结果:CHN 具有抗氧化和抗炎特性,能有效抵消 CPF 引起的促黄体生成素(LH)、血清睾酮、卵泡刺激素(FSH)和睾丸酶生物标志物的降低。此外,CHN 还能增强抗氧化防御能力,下丘脑、睾丸和附睾中丙二醛 (MDA) 含量的降低和谷胱甘肽 (GSH) 含量的增加都证明了这一点。与仅使用氯化石蜡组相比,联合使用 CHN 组的一氧化氮(NO)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)等炎症指标显著降低。组织病理学分析证实了 CHN 对组织完整性的保护作用:菊粉纳米晶体具有抗炎和抗氧化特性,在缓解氯化石蜡诱导的雄性大鼠生殖缺陷方面具有良好的潜力。这项研究为针对环境毒素引起的生殖毒性的治疗干预提供了有价值的见解,强调了纳米菊粉作为一种保护剂在氯化石蜡暴露情况下的潜力。
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引用次数: 0
Mutations in Rv0678, Rv2535c, and Rv1979c Confer Resistance to Bedaquiline in Clinical Isolates of Mycobacterium Tuberculosis. Rv0678、Rv2535c 和 Rv1979c 基因突变导致临床结核分枝杆菌对贝达喹啉产生耐药性。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429314641240815080447
Khaoula Balgouthi, Manaf AlMatar, Hamza Saghrouchni, Osman Albarri, Işıl Var

Introduction: Reduced bedaquiline (BDQ) sensitivity to antimycobacterial drugs has been linked to mutations in the Rv0678, pepQ, and Rv1979c genes of Mycobacterium tuberculosis (MTB). Resistance-causing mutations in MTB strains under treatment may have an impact on novel BDQ-based medication regimens intended to reduce treatment time. Due to this, we investigated the genetic basis of BDQ resistance in Turkish TB patients with MTB clinical isolates. Furthermore, mutations in the genes linked to efflux pumps were examined as a backup resistance mechanism.

Methods: We scrutinized 100 MTB clinical isolates from TB patients using convenience sampling. Eighty MDR and twenty pan-drug susceptible MTB strains were among these isolates. Sequencing was performed on all strains, and genomic analyses were performed to find mutations in BDQ resistance-associated genes, including Rv0678 and pepQ(Rv2535c), which correspond to a putative Xaa-Pro aminopeptidase, and Rv1979c. Of the 74 isolates with PepQ (Rv2535c) mutations, four isolates (2.96%) exhibited MGIT-BDQ susceptibility.

Results: Twenty-one (19.11%) of the ninety-one isolates carrying mutations, including Rv1979c, were MGIT-BDQ-sensitive. Nonetheless, out of the 39 isolates with Rv0678 mutations, four (2.96%) were sensitive to MGIT-BDQ. It was found that resistance-associated variants (RAVs) in Rv0678, pepQ, and Rv1979c are often linked to BDQ resistance.

Conclusion: In order to include variations in efflux pump genes in genome-based diagnostics for drug-resistant MTB, further evidence about their involvement in resistance is needed.

导言:结核分枝杆菌(MTB)的 Rv0678、epQ 和 Rv1979c 基因突变与贝达喹啉(BDQ)对抗结核药物的敏感性降低有关。正在接受治疗的 MTB 菌株中的致耐药性突变可能会对旨在缩短治疗时间的基于 BDQ 的新型药物治疗方案产生影响。因此,我们研究了土耳其肺结核患者临床分离的 MTB 菌株对 BDQ 产生耐药性的基因基础。此外,我们还将与外排泵相关的基因突变作为一种后备耐药机制进行了研究:方法:我们采用便利抽样法仔细检查了来自结核病患者的 100 例 MTB 临床分离株。这些分离株中有 80 株 MDR MTB 和 20 株泛药敏 MTB。我们对所有菌株进行了测序,并通过基因组分析发现了 BDQ 耐药性相关基因的突变,包括 Rv0678 和 pepQ(Rv2535c)(对应于一种假定的 Xaa-Pro 氨基肽酶)以及 Rv1979c。在 PepQ(Rv2535c)突变的 74 个分离株中,有 4 个分离株(2.96%)表现出对 MGIT-BDQ 的敏感性:结果:在包括 Rv1979c 在内的 91 个携带突变的分离株中,有 21 个(19.11%)对 MGIT-BDQ 敏感。然而,在 39 个携带 Rv0678 突变的分离株中,有 4 个(2.96%)对 MGIT-BDQ 敏感。研究发现,Rv0678、pepQ 和 Rv1979c 中的抗性相关变异(RAVs)往往与 BDQ 抗性有关:结论:为了将外排泵基因变异纳入耐药 MTB 的基因组诊断中,需要进一步证明它们与耐药性的关系。
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引用次数: 0
Fenofibrate Inhibits LPS and Zymosan-induced Inflammatory Responses through Sonic Hedgehog in IMG Cells. 非诺贝特通过Sonic Hedgehog基因抑制LPS和zymosan诱导的IMG细胞炎症反应。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429317532241017051135
Yu-Wen Wang, Bor-Ren Huang, Dah-Yuu Lu, Jin-Wun Chen, Vichuda Charoensaensuk, Liang-Yo Yang, Sheng-Wei Lai, Cheng-Fang Tsai, Wei-Lan Yeh

Background: Neuroinflammatory responses are strongly associated with the pathogenesis of progressive neurodegenerative conditions and mood disorders. Modulating microglial activation is a potential strategy for developing protective treatments for central nervous system (CNS)-related diseases. Fibrates, widely used in clinical practice as cholesterol-lowering medications, exhibit numerous biological activities, such as anticancer and antiinflammatory activities. However, the mechanisms underlying their beneficial effects on the CNS remain unclear.

Objective: This study investigated the mechanisms through which fibrates influence inflammatory and anti-inflammatory homeostasis in microglial cells.

Methods: Cell viability assay, nitric oxide measurement, Western blot analysis,, real-time PCR, and cell transfection were used in this study.

Results: Fenofibrate, a well-known fibrate, reduced the production of nitric oxide and interleukin-6 and the expression of inducible nitric oxide synthase and cyclooxygenase-2 in microglial cells. It also inhibited the expression of various proinflammatory cytokines and chemokines, including tumor necrosis factor-ɑ and interleukin-1β, and chemokine (C-C) motif ligand 2 and chemokine (C-X-C motif) ligand 10. Notably, treatment of fenofibrate dramatically activated the sonic hedgehog (SHH) and sirtuin-1 (SIRT1). Furthermore, the inhibition of SHH or SIRT1 mitigated the anti-inflammatory effects of fenofibrate in IMG microglial cells.

Conclusion: Our findings suggest that fenofibrate may inhibit inflammatory responses by activating SIRT1 and SHH in IMG microglial cells. Our study suggests that fenofibrate or targeting SHH molecule is a promising therapeutic strategy for neuroinflammation-associated conditions. Further research with additional cell lines and in vivo models is needed to understand its therapeutic potential.

背景:神经炎症反应与进行性神经退行性疾病和情绪障碍的发病机制密切相关。调节小胶质细胞激活是开发中枢神经系统(CNS)相关疾病保护性治疗的潜在策略。贝特类药物作为降胆固醇药物广泛应用于临床,具有多种生物活性,如抗癌和抗炎活性。然而,它们对中枢神经系统有益作用的机制尚不清楚。目的:探讨贝特类药物影响小胶质细胞炎症和抗炎稳态的机制。方法:采用细胞活力测定、一氧化氮测定、Western blot分析、实时荧光定量PCR、细胞转染等方法。结果:非诺贝特能降低小胶质细胞中一氧化氮和白细胞介素-6的生成以及诱导型一氧化氮合酶和环氧合酶-2的表达。它还抑制多种促炎细胞因子和趋化因子的表达,包括肿瘤坏死因子和白细胞介素-1,趋化因子(C-C)基序配体2和趋化因子(C-X-C基序)配体10。值得注意的是,非诺贝特治疗显著激活了超音hedgehog基因(SHH)和sirtuin-1 (SIRT1)。此外,SHH或SIRT1的抑制减轻了非诺贝特在IMG小胶质细胞中的抗炎作用。结论:本研究提示非诺贝特可能通过激活IMG小胶质细胞中的SIRT1和SHH来抑制炎症反应。我们的研究表明,非诺贝特或靶向SHH分子是一种很有前途的治疗神经炎症相关疾病的策略。需要更多细胞系和体内模型的进一步研究来了解其治疗潜力。
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引用次数: 0
The Role of Local Angiotensin II/Angiotensin Type 1 Receptor in Endometriosis: A Potential Target for New Treatment Approaches 局部血管紧张素 II/血管紧张素 1 型受体在子宫内膜异位症中的作用:新治疗方法的潜在目标。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429315431240712100124
Shirin Moazen, Mohammad-Hassan Arjmand

Endometriosis is a chronic inflammatory disorder described by the presence of functional endometrial-like tissues at extra-uterine locations that are related to chronic pelvic pain and infertility. Multiple molecular mechanisms, including inflammation, reactive oxygen species (ROS) generation, fibrotic reactions, and angiogenesis, are involved in the pathogenesis of endometriosis; however, the exact cause of this disorder still remains a matter of discussion. Recently, it has been shown that the local renin-angiotensin system (RAS) has been expressed in different tissues, like the gynecological tract, and alterations in its expression are associated with multiple pathological conditions like endometriosis. Angiotensin II (Ang II), as a main peptide of the RAS through angiotensin type 1 receptor (AT1R), upregulates signal transduction pathways such as nuclear factor kappa B (NF-κB), mitogen activation protein kinase (MAPK), and transforming growth factor beta (TGF-β) to promote inflammation, oxidative stress, and fibrogenesis. Angiotensin receptor blockers (ARBs) control high blood pressure, which is increased by excessive AT1R activity. Recently, it has been recognized that ARBs have tissue protective effects because of their anti-inflammatory and antifibrotic effects. In this review, we focused on the role of local Ang II/AT1R axis activity in endometriosis pathogenesis and justified the use of ARB agents as a potential therapeutic strategy to improve endometriosis.

子宫内膜异位症是一种慢性炎症性疾病,其特征是在子宫外位置存在功能性子宫内膜样组织,与慢性盆腔疼痛和不孕症有关。包括炎症、活性氧(ROS)生成、纤维化反应和血管生成在内的多种分子机制参与了子宫内膜异位症的发病机制;然而,这种疾病的确切病因仍是一个有待讨论的问题。最近的研究表明,局部肾素-血管紧张素系统(RAS)在妇科等不同组织中均有表达,其表达的改变与子宫内膜异位症等多种病症有关。血管紧张素 II(Ang II)作为 RAS 的主要肽,通过血管紧张素 1 型受体(AT1R)上调核因子卡巴 B(NF-κB)、丝裂原活化蛋白激酶(MAPK)和转化生长因子 beta(TGF-β)等信号转导通路,从而促进炎症、氧化应激和纤维增生。血管紧张素受体阻滞剂(ARB)可控制因 AT1R 活性过高而升高的高血压。最近,人们认识到血管紧张素受体阻滞剂因其抗炎和抗纤维化作用而具有组织保护作用。在这篇综述中,我们重点探讨了局部Ang II/AT1R轴活性在子宫内膜异位症发病机制中的作用,并论证了使用ARB药物作为改善子宫内膜异位症的潜在治疗策略的合理性。
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引用次数: 0
Upregulation of LncRNA WT1-AS Inhibits Tumor Growth and Promotes Autophagy in Gastric Cancer via Suppression of PI3K/Akt/mTOR Pathway. 通过抑制 PI3K/Akt/mTOR 通路,上调 LncRNA WT1-AS 可抑制胃癌中的肿瘤生长并促进自噬。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429318398240918063450
Xiaobei Zhang, Meng Jin, Xiaoying Yao, Jilan Liu, Yonghong Yang, Jian Huang, Guiyuan Jin, Shiqi Liu, Baogui Zhang

Background: Increasing evidence has highlighted the involvement of the imbalance of long non-coding RNAs in the development of gastric cancer (GC), which is one of the most common malignancies in the world. This study aimed to determine the role of lncRNA WT1-AS in the progression of GC and explore its underlying mechanism.

Methods: The expression of lncRNA WT1-AS in gastric cancer tissues was detected using RT-qPCR. We knocked down the expression of WT1-AS in GC cells or treated them with rapamycin or both. Then, transwell assay and scratch assay were carried out to determine the migration of GC cells, and flow cytometry was carried out to determine the cell cycle. The immunofluorescence technique was used to determine the autophagy, and a tumor formation experiment was carried out to determine tumor growth in vivo. The expression of factors related to the PI3K/Akt/mTOR pathway was also measured by Western Blotting.

Results: In GC tissues and cells, lncRNA WT1-AS was underexpressed. Moreover, overexpression of lncRNA WT1-AS blocked the PI3K/Akt/mTOR pathway. Upregulation of lncRNA WT1-AS or inhibition of the PI3K/Akt/mTOR pathway suppressed cancer cell migration in vitro, leading to cell cycle arrest, and promoted autophagy while inhibiting tumor growth in vivo. It also reduced the expression levels of Ki-67, MMP2, MMP9, and VEGF. The WT1-AS+rapamycin group was the most prominent in all experiments.

Conclusion: The upregulation of lncRNA WT1-AS could suppress the PI3K/Akt/mTOR pathway, which inhibits cell migration and cell cycle arrest while promoting autophagy in gastric cancer cells.

背景:越来越多的证据表明,胃癌(GC)是世界上最常见的恶性肿瘤之一,长非编码RNA的失衡参与了胃癌的发病。本研究旨在确定lncRNA WT1-AS在GC进展中的作用并探索其潜在机制:方法:采用RT-qPCR技术检测lncRNA WT1-AS在胃癌组织中的表达。我们敲除了 WT1-AS 在 GC 细胞中的表达,或用雷帕霉素处理细胞,或同时用雷帕霉素和雷帕霉素处理细胞。然后,我们进行了Transwell试验和划痕试验以测定GC细胞的迁移,并用流式细胞术测定细胞周期。免疫荧光技术用于检测自噬情况,肿瘤形成实验用于检测体内肿瘤生长情况。此外,还通过 Western 印迹法测定了 PI3K/Akt/mTOR 通路相关因子的表达:结果:在GC组织和细胞中,lncRNA WT1-AS表达不足。此外,过表达 lncRNA WT1-AS 会阻断 PI3K/Akt/mTOR 通路。上调lncRNA WT1-AS或抑制PI3K/Akt/mTOR通路可抑制体外癌细胞迁移,导致细胞周期停滞,促进自噬,同时抑制体内肿瘤生长。它还能降低 Ki-67、MMP2、MMP9 和 VEGF 的表达水平。WT1-AS+拉帕霉素组在所有实验中表现最为突出:lncRNA WT1-AS的上调可抑制PI3K/Akt/mTOR通路,从而抑制细胞迁移和细胞周期停滞,同时促进胃癌细胞的自噬。
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引用次数: 0
Adipose Tissue Dysfunction Following Trauma and Hypoxia Increases the Risk of Post-Surgical Adhesion: Potential for Therapeutic Interventions 创伤和缺氧后的脂肪组织功能障碍会增加手术后粘连的风险:治疗干预的潜力。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429308567240806111848
Rozita Khodashahi, Mahmoud Tavakkoli, Gorgon A Ferns, Leyla Feyzmohammadi, Amir Hossein Mirzaei, Mohsen Aliakbarian, Mohammad-Hassan Arjmand

Post-surgical adhesion is a medical challenge, especially following abdominal and pelvic surgeries. This refers to the formation of fibrotic scars that form from connective tissue in the gynecological tract or abdominal cavity. Dysfunctional adipose tissue (AT) by surgical injuries and hypoxia increases the risk of post-surgical adhesion through different molecular mechanisms. Damage-associated molecular patterns (DAMPs) and Hypoxia-induced factor 1 alpha (HIF-1α) produced during surgery trauma and hypoxia induce AT dysfunction to promote inflammation, oxidative stress, metabolic alterations, and profibrotic pathways, which contribute to post-surgical adhesions. HIF-1α and DAMPs can be considered therapeutic targets to prevent AT dysfunction and diminish the formation of adhesions in obese patients undergoing abdominal or pelvic surgeries.

手术后粘连是一项医学难题,尤其是在腹部和盆腔手术后。这是指妇科腔道或腹腔内结缔组织形成的纤维化疤痕。手术损伤和缺氧导致的脂肪组织(AT)功能失调会通过不同的分子机制增加手术后粘连的风险。手术创伤和缺氧过程中产生的损伤相关分子模式(DAMPs)和缺氧诱导因子 1α(HIF-1α)会诱发脂肪组织功能障碍,从而促进炎症、氧化应激、代谢改变和组织坏死通路,导致手术后粘连。HIF-1α和DAMPs可被视为治疗靶点,以防止腹部或盆腔手术肥胖患者的AT功能障碍并减少粘连的形成。
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引用次数: 0
Mass Spectrometry in Covalent Drug Discovery. 质谱法在共价药物发现中的应用。
Pub Date : 2024-01-01 DOI: 10.2174/0118761429319065240605104628
Chang Liu, Xiujuan Wen
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引用次数: 0
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Current molecular pharmacology
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