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Methane saline suppresses ferroptosis via the Nrf2/HO-1 signaling pathway to ameliorate intestinal ischemia-reperfusion injury. 甲烷生理盐水通过Nrf2/HO-1信号通路抑制铁突变,从而改善肠道缺血再灌注损伤。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-07-18 DOI: 10.1080/13510002.2024.2373657
Qingrui Fan, Hulin Chang, Lifei Tian, Bobo Zheng, Ruiting Liu, Zeyu Li

Objectives: Intestinal ischemia-reperfusion (I/R) injury is a multifactorial and complex clinical pathophysiological process. Current research indicates that the pathogenesis of intestinal I/R injury involves various mechanisms, including ferroptosis. Methane saline (MS) has been demonstrated to primarily exert anti-inflammatory and antioxidant effects in I/R injury. In this study, we mainly investigated the effect of MS on ferroptosis in intestinal I/R injury and determined its potential mechanism.

Methods: In vivo and in vitro intestinal I/R injury models were established to validate the relationship between ferroptosis and intestinal I/R injury. MS treatment was applied to assess its impact on intestinal epithelial cell damage, intestinal barrier disruption, and ferroptosis.

Results: MS treatment led to a reduction in I/R-induced intestinal epithelial cell damage and intestinal barrier disruption. Moreover, similar to treatment with ferroptosis inhibitors, MS treatment reduced ferroptosis in I/R, as indicated by a decrease in the levels of intracellular pro-ferroptosis factors, an increase in the levels of anti-ferroptosis factors, and alleviation of mitochondrial damage. Additionally, the expression of Nrf2/HO-1 was significantly increased after MS treatment. However, the intestinal protective and ferroptosis inhibitory effects of MS were diminished after the use of M385 to inhibit Nrf2 in mice or si-Nrf2 in Caco-2 cells.

Discussion: We proved that intestinal I/R injury was mitigated by MS and that the underlying mechanism involved modulating the Nrf2/HO-1 signaling pathway to decrease ferroptosis. MS could be a promising treatment for intestinal I/R injury.

目的:肠缺血再灌注(I/R)损伤是一种多因素、复杂的临床病理生理学过程。目前的研究表明,肠缺血再灌注损伤的发病机制涉及多种机制,包括铁变态反应。甲烷生理盐水(MS)已被证实在 I/R 损伤中主要发挥抗炎和抗氧化作用。本研究主要探讨了 MS 对肠 I/R 损伤中铁细胞凋亡的影响,并确定了其潜在机制:方法:建立体内和体外肠道 I/R 损伤模型,验证铁蛋白沉积与肠道 I/R 损伤之间的关系。方法:建立体内和体外肠道 I/R 损伤模型,验证铁蛋白沉积与肠道 I/R 损伤之间的关系;应用 MS 治疗,评估其对肠道上皮细胞损伤、肠道屏障破坏和铁蛋白沉积的影响:结果:MS治疗可减少I/R引起的肠上皮细胞损伤和肠屏障破坏。此外,与使用铁蛋白沉积抑制剂类似,MS治疗也能减少I/R中的铁蛋白沉积,表现为细胞内促铁蛋白沉积因子水平的降低、抗铁蛋白沉积因子水平的升高以及线粒体损伤的减轻。此外,MS治疗后Nrf2/HO-1的表达明显增加。然而,在使用M385抑制小鼠Nrf2或在Caco-2细胞中使用si-Nrf2后,MS的肠道保护和铁突变抑制作用减弱:讨论:我们证明了MS可减轻肠道I/R损伤,其基本机制涉及调节Nrf2/HO-1信号通路以减少铁卟啉沉积。MS可能是一种治疗肠道I/R损伤的有效方法。
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引用次数: 0
Bilirubin regulates cell death type by alleviating macrophage mitochondrial dysfunction caused by cigarette smoke extract. 胆红素通过缓解香烟烟雾提取物导致的巨噬细胞线粒体功能障碍来调节细胞死亡类型。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-07-29 DOI: 10.1080/13510002.2024.2382946
Jingjing Wei, Yuan Tian, Jinshu Wei, Meiqi Guan, Xiaoya Yu, Jianing Xie, Guoquan Fan

Objectives: To explore the effects and mechanisms of bilirubin on mitochondrial function and type of macrophage cell death after exposure to cigarette smoke extract (CSE).

Methods: RAW264.7 macrophages were treated with different concentrations of CSE and bilirubin solutions and divided into four groups: control, CSE, bilirubin, and bilirubin + CSE groups. The necrotic and apoptotic states of the macrophages were determined using an Annexin V-fluorescein 5-isothiocyanate/propidium iodide (FITC/PI) staining kit. Cytoplasmic NOD-like receptor family, pyrin domain containing 3 (NLRP3) expression in macrophages was detected by immunofluorescence and the levels of IL-1β and IL-18 in the supernatants of culture medium were detected by enzyme linked immunosorbent assay (ELISA) test. A JC-1 mitochondrial membrane potential detection kit was used to assess mitochondrial membrane damage and the adenosine triphosphate (ATP) assay kit was used to determine intracellular ATP levels. After the macrophages were stained with reactive oxygen species (ROS) specific dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA), the fluorescence intensity and proportion of ROS-positive macrophages were measured using flow cytometry.

Results: We observed that compared with those of 0 μM (control group), concentrations of 5, 10, or 20 μΜ bilirubin significantly decreased cell viability, which was increased by bilirubin exposure below 1 μM. The effect of CSE on macrophage viability was concentration- and time-dependent. Bilirubin of 0.2 μM could alleviate the inhibition of macrophage viability caused by 5% CSE. In addition, bilirubin intervention could reduce the occurrence of necrosis and pyroptosis to a certain extent.

Conclusions: CSE could cause mitochondrial dysfunction in macrophages, as demonstrated by a decrease in mitochondrial membrane potential and intracellular ATP levels and an increase in ROS production, while bilirubin could relieve mitochondrial dysfunction caused by CSE.

目的探讨胆红素对线粒体功能的影响和机制,以及暴露于香烟烟雾提取物(CSE)后巨噬细胞的死亡类型:用不同浓度的 CSE 和胆红素溶液处理 RAW264.7 巨噬细胞,将其分为四组:对照组、CSE 组、胆红素组和胆红素 + CSE 组。巨噬细胞的坏死和凋亡状态由 Annexin V 荧光素-5-异硫氰酸盐/碘化丙啶(FITC/PI)染色试剂盒测定。通过免疫荧光检测巨噬细胞中细胞质 NOD 样受体家族、含吡啶域 3(NLRP3)的表达,并通过酶联免疫吸附试验(ELISA)检测培养基上清液中 IL-1β 和 IL-18 的水平。JC-1 线粒体膜电位检测试剂盒用于评估线粒体膜损伤,三磷酸腺苷(ATP)检测试剂盒用于测定细胞内 ATP 水平。用活性氧(ROS)特异性染料--2',7'-二氯二氢荧光素二乙酸酯(DCFH-DA)对巨噬细胞进行染色后,用流式细胞仪测量ROS阳性巨噬细胞的荧光强度和比例:我们观察到,与 0 μM(对照组)相比,浓度为 5、10 或 20 μΜ 的胆红素会显著降低细胞活力,而浓度低于 1 μM 的胆红素会增加细胞活力。CSE 对巨噬细胞活力的影响与浓度和时间有关。0.2 μM 的胆红素可减轻 5% CSE 对巨噬细胞活力的抑制。此外,胆红素的干预还能在一定程度上减少巨噬细胞坏死和脓毒症的发生:结论:CSE 可导致巨噬细胞线粒体功能障碍,表现为线粒体膜电位和细胞内 ATP 水平下降以及 ROS 生成增加,而胆红素可缓解 CSE 导致的线粒体功能障碍。
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引用次数: 0
Navigating the redox landscape: reactive oxygen species in regulation of cell cycle. 氧化还原景观导航:活性氧对细胞周期的调控。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-07-07 DOI: 10.1080/13510002.2024.2371173
Viktoria Mackova, Martina Raudenska, Hana Holcova Polanska, Milan Jakubek, Michal Masarik

Objectives: To advance our knowledge of disease mechanisms and therapeutic options, understanding cell cycle regulation is critical. Recent research has highlighted the importance of reactive oxygen species (ROS) in cell cycle regulation. Although excessive ROS levels can lead to age-related pathologies, ROS also play an essential role in normal cellular functions. Many cell cycle regulatory proteins are affected by their redox status, but the precise mechanisms and conditions under which ROS promote or inhibit cell proliferation are not fully understood.Methods: This review presents data from the scientific literature and publicly available databases on changes in redox state during the cell cycle and their effects on key regulatory proteins.Results: We identified redox-sensitive targets within the cell cycle machinery and analysed different effects of ROS (type, concentration, duration of exposure) on cell cycle phases. For example, moderate levels of ROS can promote cell proliferation by activating signalling pathways involved in cell cycle progression, whereas excessive ROS levels can induce DNA damage and trigger cell cycle arrest or cell death.Discussion: Our findings encourage future research focused on identifying redox-sensitive targets in the cell cycle machinery, potentially leading to new treatments for diseases with dysregulated cell proliferation.

目的:为了增进我们对疾病机理和治疗方案的了解,了解细胞周期调控至关重要。最近的研究强调了活性氧(ROS)在细胞周期调控中的重要性。虽然过高的 ROS 水平会导致与年龄相关的病症,但 ROS 在正常细胞功能中也发挥着至关重要的作用。许多细胞周期调控蛋白受其氧化还原状态的影响,但 ROS 促进或抑制细胞增殖的确切机制和条件尚未完全明了:本综述介绍了科学文献和公开数据库中有关细胞周期中氧化还原状态变化及其对关键调控蛋白影响的数据:我们确定了细胞周期机制中的氧化还原敏感靶标,并分析了 ROS(类型、浓度、暴露持续时间)对细胞周期各阶段的不同影响。例如,中等水平的氧化还原反应可通过激活细胞周期进展的信号通路促进细胞增殖,而过量的氧化还原反应则会诱发DNA损伤,引发细胞周期停滞或细胞死亡:我们的研究结果鼓励未来的研究重点放在确定细胞周期机制中对氧化还原反应敏感的靶点上,这有可能为细胞增殖失调疾病带来新的治疗方法。
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引用次数: 0
Hyperoxia exposure induces ferroptosis and apoptosis by downregulating PLAGL2 and repressing HIF-1α/VEGF signaling pathway in newborn alveolar typeII epithelial cell. 高氧暴露通过下调PLAGL2和抑制新生肺泡II型上皮细胞的HIF-1α/VEGF信号通路,诱导铁变态和细胞凋亡。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-08-05 DOI: 10.1080/13510002.2024.2387465
Yuting Zhu, Hongmei Hou, Yawen Li, Yanyu Zhang, Yuanyuan Fang, Si Chen, Le Zhang, Weilai Jin, Yahui Zhou

Backgroud: Bronchopulmonary dysplasia (BPD) is one of the most important complications plaguing neonates and can lead to a variety of sequelae. the ability of the HIF-1α/VEGF signaling pathway to promote angiogenesis has an important role in neonatal lung development.

Method: Newborn rats were exposed to 85% oxygen. The effects of hyperoxia exposure on Pleomorphic Adenoma Gene like-2 (PLAGL2) and the HIF-1α/VEGF pathway in rats lung tissue were assessed through immunofluorescence and Western Blot analysis. In cell experiments, PLAGL2 was upregulated, and the effects of hyperoxia and PLAGL2 on cell viability were evaluated using scratch assays, CCK-8 assays, and EDU staining. The role of upregulated PLAGL2 in the HIF-1α/VEGF pathway was determined by Western Blot and RT-PCR. Apoptosis and ferroptosis effects were determined through flow cytometry and viability assays.

Results: Compared with the control group, the expression levels of PLAGL2, HIF-1α, VEGF, and SPC in lung tissues after 3, 7, and 14 days of hyperoxia exposure were all decreased. Furthermore, hyperoxia also inhibited the proliferation and motility of type II alveolar epithelial cells (AECII) and induced apoptosis in AECII. Upregulation of PLAGL2 restored the proliferation and motility of AECII and suppressed cell apoptosis and ferroptosis, while the HIF-1α/VEGF signaling pathway was also revived.

Conclusions: We confirmed the positive role of PLAGL2 and HIF-1α/VEGF signaling pathway in promoting BPD in hyperoxia conditions, and provided a promising therapeutic targets.

背景:支气管肺发育不良(BPD)是困扰新生儿的最重要的并发症之一,可导致多种后遗症。HIF-1α/VEGF信号通路促进血管生成的能力在新生儿肺发育中具有重要作用:方法:将新生大鼠暴露于 85% 的氧气中。方法:通过免疫荧光和 Western Blot 分析评估高氧暴露对大鼠肺组织中 Pleomorphic Adenoma Gene like-2 (PLAGL2) 和 HIF-1α/VEGF 通路的影响。在细胞实验中,PLAGL2 被上调,并通过划痕实验、CCK-8 实验和 EDU 染色评估了高氧和 PLAGL2 对细胞活力的影响。通过 Western Blot 和 RT-PCR 测定了上调的 PLAGL2 在 HIF-1α/VEGF 通路中的作用。通过流式细胞术和存活率测定确定了凋亡和铁凋亡效应:结果:与对照组相比,高氧暴露 3、7 和 14 天后,肺组织中 PLAGL2、HIF-1α、VEGF 和 SPC 的表达水平均下降。此外,高氧还抑制了 II 型肺泡上皮细胞(AECII)的增殖和运动,并诱导了 AECII 的凋亡。PLAGL2的上调恢复了肺泡上皮细胞的增殖和运动,抑制了细胞凋亡和铁凋亡,同时HIF-1α/VEGF信号通路也恢复了活力:结论:我们证实了 PLAGL2 和 HIF-1α/VEGF 信号通路在高氧条件下促进 BPD 的积极作用,并提供了一个很有前景的治疗靶点。
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引用次数: 0
Sarmentosin alleviates doxorubicin-induced cardiotoxicity and ferroptosis via the p62-Keap1-Nrf2 pathway. 沙门托品通过p62-Keap1-Nrf2途径减轻多柔比星诱导的心脏毒性和铁变态反应
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-08-16 DOI: 10.1080/13510002.2024.2392329
Zhihui Lin, Chang Wu, Dongyan Song, Chenxi Zhu, Bosen Wu, Jie Wang, Yangjing Xue

Doxorubicin (Dox) is extensively used as an antitumor agent, but its severe cardiotoxicity significantly limits its clinical use. Current treatments for Dox-induced cardiotoxicity are inadequate, necessitating alternative solutions. This study evaluated the effects of sarmentosin, a compound from Sedum sarmentosum, on Dox-induced cardiotoxicity and dysfunction. Sarmentosin was administered as a pretreatment to both mice and H9c2 cells before Dox exposure. Subsequently, markers of Dox-induced cardiotoxicity and ferroptosis in serum and cell supernatants were measured. Western blot analysis was utilized to detect levels of ferroptosis, oxidative stress, and autophagy proteins. Additionally, echocardiography, hematoxylin-eosin staining, ROS detection, and immunofluorescence techniques were employed to support our findings. Results demonstrated that sarmentosin significantly inhibited iron accumulation, lipid peroxidation, and oxidative stress, thereby reducing Dox-induced ferroptosis and cardiotoxicity in C57BL/6 mice and H9c2 cells. The mechanism involved the activation of autophagy and the Nrf2 signaling pathway. These findings suggest that sarmentosin may prevent Dox-induced cardiotoxicity by mitigating ferroptosis. The study underscores the potential of compounds like sarmentosin in treating Dox-induced cardiotoxicity.

多柔比星(Dox)被广泛用作抗肿瘤药物,但其严重的心脏毒性极大地限制了其临床应用。目前针对 Dox 引起的心脏毒性的治疗方法并不完善,因此需要其他解决方案。本研究评估了沙门菌素(一种从沙门菌中提取的化合物)对 Dox 诱导的心脏毒性和功能障碍的影响。在暴露于 Dox 之前,对小鼠和 H9c2 细胞进行沙门菌素预处理。随后,测量了血清和细胞上清液中由 Dox 诱导的心脏毒性和铁中毒的标记物。利用 Western 印迹分析检测铁变态反应、氧化应激和自噬蛋白的水平。此外,还采用了超声心动图、苏木精-伊红染色、ROS 检测和免疫荧光技术来支持我们的研究结果。结果表明,沙门托品能显著抑制铁积累、脂质过氧化和氧化应激,从而减轻Dox诱导的C57BL/6小鼠和H9c2细胞的铁中毒和心脏毒性。其机制涉及自噬和 Nrf2 信号通路的激活。这些研究结果表明,沙门托品可通过减轻铁卟啉沉积来预防Dox诱导的心脏毒性。这项研究强调了沙门菌素等化合物在治疗 Dox 诱导的心脏毒性方面的潜力。
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引用次数: 0
Therapeutic potential of EVs loaded with CB2 receptor agonist in spinal cord injury via the Nrf2/HO-1 pathway. 含有 CB2 受体激动剂的 EVs 通过 Nrf2/HO-1 途径对脊髓损伤的治疗潜力。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-10-28 DOI: 10.1080/13510002.2024.2420572
Imran Ibrahim Shaikh, Ramesh Bhandari, Shekhar Singh, Xu Zhu, Khawar Ali Shahzad, Chuxiao Shao, Liming Cheng, Jian Xiao

Background: Spinal cord injury (SCI) poses a challenge due to limited treatment options. Recently, the effect and mechanism of Exo-loaded cannabinoid receptor type 2 (CB2) agonist AM1241(Exo + AM1241) have been applied in other inflammatory diseases but not in SCI.

Methods: The SCI model was set up using C57BL/6 mice, followed by the treatment of Exo, AM1241, and Exo + AM1241. We assessed the effects of the following treatments on motor function recovery using BMS, and evaluated histological changes, apoptosis activity, inflammation, and oxidative stress in the SCI mice model. Additionally, the effect of following treatments on spinal cord neural stem cells (NSCs) was evaluated under lipopolysaccharides (LPS) induced inflammatory and oxidative models and, glutamate (Gluts) induced cell apoptosis models.

Result: Our results demonstrated that Exo + AM1241 treatment significantly improved motor function recovery, after SCI by decreasing proinflammatory cytokines, and suppressing astrocyte/microglia (GFAP/Iba1) activation in the injury zone. Additionally, this treatment reduces pro-apoptotic proteins (Bax and caspase 3), increases the levels of the anti-apoptotic protein Bcl-2, enhances antioxidant defenses by boosting SOD and GSH, and lowers oxidative stress markers such as MDA. It also activates the Nuclear factor erythroid-2 (Nrf2) related factor 2 signaling pathway, thereby enhancing tissue protection against damage and cell death.

背景:脊髓损伤(SCI)因治疗方案有限而成为一项挑战。最近,外载大麻素受体 2 型(CB2)激动剂 AM1241(Exo + AM1241)的作用和机制已被应用于其他炎症性疾病,但尚未应用于 SCI:方法:使用 C57BL/6 小鼠建立 SCI 模型,然后使用 Exo、AM1241 和 Exo + AM1241 治疗。我们使用 BMS 评估了后续治疗对运动功能恢复的影响,并评估了 SCI 小鼠模型的组织学变化、细胞凋亡活性、炎症和氧化应激。此外,在脂多糖(LPS)诱导的炎症和氧化模型以及谷氨酸(Gluts)诱导的细胞凋亡模型下,评估了以下治疗方法对脊髓神经干细胞(NSCs)的影响:结果:我们的研究结果表明,Exo + AM1241 治疗通过减少促炎细胞因子和抑制损伤区星形胶质细胞/小胶质细胞(GFAP/Iba1)的激活,明显改善了 SCI 后的运动功能恢复。此外,这种疗法还能减少促凋亡蛋白(Bax 和 caspase 3),提高抗凋亡蛋白 Bcl-2 的水平,通过提高 SOD 和 GSH 来增强抗氧化防御能力,并降低氧化应激指标(如 MDA)。它还能激活核因子红细胞-2(Nrf2)相关因子 2 信号通路,从而增强组织对损伤和细胞死亡的保护。
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引用次数: 0
Evaluating anticancer activity of emodin by enhancing antioxidant activities and affecting PKC/ADAMTS4 pathway in thioacetamide-induced hepatocellular carcinoma in rats. 评估大黄素通过增强抗氧化活性和影响PKC/ADAMTS4通路对硫代乙酰胺诱导的大鼠肝细胞癌的抗癌活性
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-06-11 DOI: 10.1080/13510002.2024.2365590
Hanan M Hassan, Ahmed M Hamdan, Abdullah Alattar, Reem Alshaman, Omar Bahattab, Mohammed M H Al-Gayyar

Emodin is a naturally occurring anthraquinone derivative with a wide range of pharmacological activities, including neuroprotective and anti-inflammatory activities. We aim to assess the anticancer activity of emodin against hepatocellular carcinoma (HCC) in rat models using the proliferation, invasion, and angiogenesis biomarkers. After induction of HCC, assessment of the liver impairment and the histopathology of liver sections were investigated. Hepatic expression of both mRNA and protein of the oxidative stress biomarkers, HO-1, Nrf2; the mitogenic activation biomarkers, ERK5, PKCδ; the tissue destruction biomarker, ADAMTS4; the tissue homeostasis biomarker, aggregan; the cellular fibrinolytic biomarker, MMP3; and of the cellular angiogenesis biomarker, VEGF were measured. Emodin increased the survival percentage and reduced the number of hepatic nodules compared to the HCC group. Besides, emodin reduced the elevated expression of both mRNA and proteins of all PKC, ERK5, ADAMTS4, MMP3, and VEGF compared with the HCC group. On the other hand, emodin increased the expression of mRNA and proteins of Nrf2, HO-1, and aggrecan compared with the HCC group. Therefore, emodin is a promising anticancer agent against HCC preventing the cancer prognosis and infiltration. It works through many mechanisms of action, such as blocking oxidative stress, proliferation, invasion, and angiogenesis.

大黄素是一种天然蒽醌衍生物,具有广泛的药理活性,包括神经保护和抗炎活性。我们的目的是利用大黄素的增殖、侵袭和血管生成生物标志物评估其对大鼠肝细胞癌(HCC)模型的抗癌活性。在诱导 HCC 后,对肝损伤和肝切片组织病理学进行了评估。测定了氧化应激生物标志物 HO-1、Nrf2、有丝分裂活化生物标志物 ERK5、PKCδ、组织破坏生物标志物 ADAMTS4、组织稳态生物标志物 aggregan、细胞纤维蛋白溶解生物标志物 MMP3 和细胞血管生成生物标志物 VEGF 的肝脏 mRNA 和蛋白质表达。与HCC组相比,大黄素提高了存活率,减少了肝结节的数量。此外,与HCC组相比,大黄素降低了所有PKC、ERK5、ADAMTS4、MMP3和VEGF的mRNA和蛋白的表达。另一方面,与 HCC 组相比,大黄素增加了 Nrf2、HO-1 和 aggrecan 的 mRNA 和蛋白质的表达。因此,大黄素是一种很有前景的抗癌剂,可防止癌症的预后和浸润。大黄素通过多种作用机制发挥作用,如阻断氧化应激、增殖、侵袭和血管生成。
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引用次数: 0
CISD2 regulates oxidative stress and mitophagy to maintain the balance of the follicular microenvironment in PCOS. CISD2调节氧化应激和有丝分裂,以维持多囊卵巢综合症患者卵泡微环境的平衡。
IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-07-15 DOI: 10.1080/13510002.2024.2377870
Hong-Hui Wu, Qi Zhu, Na Liang, Yu Xiang, Tian-Yue Xu, Zi-Chao Huang, Jie-Yu Cai, Ling-Lin Weng, Hong-Shan Ge

Objectives: To observe the CISD2 expression among PCOS patients and to explore its profound impact on the follicular microenvironment. Moreover, we want to elucidate the intricate mechanistic contribution of CISD2 to the onset and progression of PCOS.

Methods: Oxidase NOX2, mitophagy-related proteins, and CISD2 were detected by WB. The changes in mitochondrial structure and quantity were observed by transmission electron microscopy. Mitochondrial and lysosome colocalization was used to detect the changes of mitophagy. MDA kit, GSH and GSSG Assay kit and ROS probe were used to detect oxidative stress damage.

Results: We found that CISD2, mitophagy and oxidase in the GCs of PCOS patients were significantly increased. Testosterone stimulation leads to the increase of oxidase, mitophagy, and CISD2 in KGN cells. CISD2 inhibition promoted the increase of mitophagy, and the activation of mitochondria-lysosome binding, while alleviating the oxidative stress.

Conclusions: Inhibition of CISD2 can improve the occurrence of oxidative stress by increasing the level of mitophagy, thus affecting the occurrence and development of PCOS diseases.

研究目的观察 CISD2 在多囊卵巢综合征患者中的表达,探讨其对卵泡微环境的深远影响。此外,我们还想阐明 CISD2 对多囊卵巢综合症发病和进展的复杂机理:方法:通过WB检测氧化酶NOX2、丝裂噬相关蛋白和CISD2。透射电子显微镜观察线粒体结构和数量的变化。线粒体和溶酶体共定位用于检测有丝分裂的变化。MDA试剂盒、GSH和GSSG检测试剂盒以及ROS探针用于检测氧化应激损伤:结果:我们发现,多囊卵巢综合征患者 GC 中的 CISD2、有丝分裂和氧化酶显著增加。睾酮刺激会导致 KGN 细胞中氧化酶、有丝分裂和 CISD2 的增加。抑制CISD2可促进有丝分裂的增加,激活线粒体与溶酶体的结合,同时缓解氧化应激:结论:抑制CISD2可通过提高有丝分裂水平来改善氧化应激的发生,从而影响多囊卵巢综合征疾病的发生和发展。
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引用次数: 0
TOM5 regulates the mitochondrial membrane potential of alveolar epithelial cells in organizing pneumonia. TOM5调节组织性肺炎中肺泡上皮细胞的线粒体膜电位。
IF 3.8 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2024-05-24 DOI: 10.1080/13510002.2024.2354625
Yan Qian, Xiao Li, Xinyu Li, Xijie Zhang, Qi Yuan, Zhengxia Wang, Minghun Zhang, Mao Huang, Ningfei Ji

Deficiency of TOM5, a mitochondrial protein, causes organizing pneumonia (OP) in mice. The clinical significance and mechanisms of TOM5 in the pathogenesis of OP remain elusive. We demonstrated that TOM5 was significantly increased in the lung tissues of OP patients, which was positively correlated with the collagen deposition. In a bleomycin-induced murine model of chronic OP, increased TOM5 was in line with lung fibrosis. In vitro, TOM5 regulated the mitochondrial membrane potential in alveolar epithelial cells. TOM5 reduced the proportion of early apoptotic cells and promoted cell proliferation. Our study shed light on the roles of TOM5 in OP.

线粒体蛋白 TOM5 缺乏会导致小鼠发生组织性肺炎(OP)。TOM5在OP发病机制中的临床意义和机制仍未确定。我们证实,TOM5 在 OP 患者的肺组织中明显增加,且与胶原沉积呈正相关。在博莱霉素诱导的小鼠慢性 OP 模型中,TOM5 的增加与肺纤维化一致。在体外,TOM5 可调节肺泡上皮细胞的线粒体膜电位。TOM5 可降低早期凋亡细胞的比例,促进细胞增殖。我们的研究揭示了TOM5在OP中的作用。
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引用次数: 0
Melittin alleviates sepsis-induced acute kidney injury by promoting GPX4 expression to inhibit ferroptosis. 美乐汀通过促进 GPX4 的表达来抑制铁变态反应,从而减轻败血症引起的急性肾损伤。
IF 3.8 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 Epub Date: 2023-12-27 DOI: 10.1080/13510002.2023.2290864
Hongyan Zan, Jizheng Liu, Meixia Yang, Honghui Zhao, Chunyan Gao, Yunyan Dai, Zhiming Wang, Hongxuan Liu, Yunfei Zhang

Objectives: Melittin, the main component of bee venom, is a natural anti-inflammatory substance, in addition to its ability to fight cancer, antiviral, and useful in diabetes treatment. This study seeks to determine whether melittin can protect renal tissue from sepsis-induced damage by preventing ferroptosis and explore the protective mechanism.

Methods: In this study, we investigated the specific protective mechanism of melittin against sepsis-induced renal injury by screening renal injury indicators and ferroptosis -related molecules and markers in animal and cellular models of sepsis.

Results: Our results showed that treatment with melittin attenuated the pathological changes in mice with lipopolysaccharide-induced acute kidney injury. Additionally, we found that melittin attenuated ferroptosis in kidney tissue by enhancing GPX4 expression, which ultimately led to the reduction of kidney tissue injury. Furthermore, we observed that melittin enhanced NRF2 nuclear translocation, which consequently upregulated GPX4 expression. our findings suggest that melittin may be a potential therapeutic agent for the treatment of sepsis-associated acute kidney injury by inhibiting ferroptosis through the GPX4/NRF2 pathway.

Conclusions: Our study reveals the protective mechanism of melittin in septic kidney injury and provides a new therapeutic direction for Sepsis-AKI.

目的:蜂毒的主要成分麦饭石素是一种天然抗炎物质,此外还具有抗癌、抗病毒和治疗糖尿病的作用。本研究旨在确定蜜滴素是否能通过阻止铁蛋白沉积来保护肾脏组织免受败血症引起的损伤,并探索其保护机制:方法:本研究通过筛选脓毒症动物模型和细胞模型中的肾损伤指标以及与铁中毒相关的分子和标记物,研究美利汀对脓毒症诱导的肾损伤的特殊保护机制:结果:我们的研究结果表明,美利汀能减轻脂多糖诱导的急性肾损伤小鼠的病理变化。此外,我们还发现,美利汀通过增强 GPX4 的表达,减轻了肾组织中的铁氧化酶活性,从而最终减轻了肾组织损伤。我们的研究结果表明,美乐汀可通过 GPX4/NRF2 途径抑制铁氧化,从而成为治疗脓毒症相关急性肾损伤的潜在治疗药物:我们的研究揭示了美乐汀在脓毒症肾损伤中的保护机制,为脓毒症急性肾损伤提供了新的治疗方向。
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Redox Report
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