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Moringa oleifera ameliorates oxidative damage caused by sodium valproate in the small intestine. 辣木可改善丙戊酸钠引起的小肠氧化损伤。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-08-01 Epub Date: 2026-01-07 DOI: 10.1080/13813455.2025.2610475
Melis Coremen, Onur Ertik, Umar Faruk Magaji, Ozlem Sacan, Omur Karabulut Bulan, Refiye Yanardag

This study aimed to investigate the protective effects of Moringa oleifera (MO) extract against valproic acid (VPA)-induced small intestine damage in rats. Forty-six adult female Sprague-Dawley rats were divided into four groups: Control (saline), MO (300 mg/kg), VPA (500 mg/kg), and VPA + MO. All treatments were administered orally for 15 days. Biochemical oxidative stress analyses revealed that MO treatment mitigated oxidative stress in VPA-treated rats. Molecular docking studies demonstrated that bioactive compounds in MO leaves exhibited potential inhibitory activity against oxidative stress-related enzymes, with high binding affinities. Immunohistochemical results indicated that VPA did not alter antioxidant stress responses such as Nrf2. However, histological examinations showed that VPA caused structural damage to the small intestine, while MO treatment alleviated this effect. Overall, MO exhibited significant protective and antioxidant properties against VPA-induced intestinal injury.

本研究旨在探讨辣木提取物对丙戊酸(VPA)致大鼠小肠损伤的保护作用。将46只成年雌性Sprague-Dawley大鼠分为4组:对照组(生理盐水)、MO (300 mg/kg)、VPA (500 mg/kg)和VPA + MO。所有治疗均口服15天。生化氧化应激分析显示,MO处理减轻了vpa处理大鼠的氧化应激。分子对接研究表明,MO叶片中的生物活性化合物对氧化应激相关酶具有潜在的抑制活性,具有较高的结合亲和力。免疫组化结果显示VPA没有改变Nrf2等抗氧化应激反应。然而,组织学检查显示VPA引起小肠结构损伤,而MO治疗减轻了这种影响。总的来说,MO对vpa诱导的肠道损伤具有显著的保护和抗氧化作用。
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引用次数: 0
2-APB restores the conditioning phenomenon in diabetic mice, exposed to cerebral ischaemia-reperfusion injury. 2-APB可恢复糖尿病小鼠脑缺血再灌注损伤后的调节现象。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-08-01 Epub Date: 2026-01-15 DOI: 10.1080/13813455.2025.2612144
Poonam Sharma, Bhupesh Sharma

Introduction: Diabetes abrogates the neuroprotection caused by ischaemic preconditioning (IPC) during cerebral ischaemia-reperfusion (CI/R) injury. The study investigates the involvement of Inositol 1,4,5-trisphosphate (IP3R) receptors in IPC-mediated neuroprotection during C/R injury in hyperglycaemic conditions.

Materials and methods: Swiss Albino mice were administered with streptozotocin (STZ) to induce diabetes. Mice were exposed to CI/R injury via common carotid arteries occlusion (20 min) followed by reperfusion (24 h). For IPC, each mouse was exposed to three-1 min cycles of ischaemia and reperfusion, followed by CI/R injury.

Results: CI/R animals showed behavioural, biochemical, and histopathological alterations. IPC was observed to attenuate the CI/R-induced detrimental effects in the normoglycemic animals; however, IPC failed to provide neuroprotection in the hyperglycaemic mice. 2-Aminoethyl diphenyl borinate (inositol 1,4,5-trisphosphate receptor (IP3R) antagonist) administration in IPC hyperglycaemic mice restored the neuroprotective effects of IPC.

Conclusion: This suggests the possible role of IP3R antagonism in IPC-mediated neuroprotection during CI/R injury in hyperglycaemic conditions.

在脑缺血再灌注(CI/R)损伤过程中,糖尿病取消了缺血预处理(IPC)对神经的保护作用。本研究探讨了肌醇1,4,5-三磷酸(IP3R)受体在高血糖状态下C/R损伤期间ipc介导的神经保护中的作用。材料与方法:采用链脲佐菌素(STZ)诱导瑞士白化病小鼠糖尿病。小鼠通过颈总动脉闭塞(20 min)再灌注(24 h)暴露于CI/R损伤。对于IPC,每只小鼠暴露于3 -1分钟的缺血和再灌注循环,然后进行CI/R损伤。结果:CI/R动物表现出行为、生化和组织病理学改变。在血糖正常的动物中,IPC可以减轻CI/ r引起的有害影响;然而,IPC不能对高血糖小鼠提供神经保护。2-氨基乙基二苯硼酸盐(肌醇1,4,5-三磷酸受体(IP3R)拮抗剂)在IPC高血糖小鼠中给予恢复IPC的神经保护作用。结论:这提示IP3R拮抗剂可能在高血糖CI/R损伤期间IP3R介导的神经保护中起作用。
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引用次数: 0
Potential benefits of Pterocarpus marsupium heartwood extract on high fat diet induced rodent model of atherosclerosis. 有袋翼柏心材提取物对高脂饮食诱导的动脉粥样硬化啮齿动物模型的潜在益处。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-08-01 Epub Date: 2026-01-07 DOI: 10.1080/13813455.2025.2610474
C Garg, B Mattoo, M A Ansari, M S Arshad, O Alam, M I Alam

Atherosclerosis, a chronic inflammatory arterial disease, involves lipid deposition and immune cell infiltration, leading to vascular thickening and dysfunction. This study evaluated the protective effects of Pterocarpus marsupium (PM) heartwood extract, rich in polyphenols and flavonoids, in a high-fat diet (HFD)-induced atherosclerosis model in male Wistar rats. Thirty-six rats were divided into six groups (n = 6), receiving either a normal or HFD, with or without atorvastatin or PM extract. After 8 weeks, hemodynamic, biochemical, oxidative stress, and inflammatory parameters were assessed, along with aortic histology. HFD-fed rats showed elevated heart rate, lipids, liver enzymes, and MDA levels, with histological signs of atherosclerosis. PM treatment significantly reduced triglyceride and MDA levels and modestly improved HDL levels. No significant changes were observed in TNF-α or IL-6. Histology revealed reduced lipid infiltration in PM-treated rats. PM extract exhibited anti-atherogenic and antioxidant effects, warranting further studies to explore its therapeutic potential in cardiovascular disease.

动脉粥样硬化是一种慢性炎症性动脉疾病,涉及脂质沉积和免疫细胞浸润,导致血管增厚和功能障碍。本研究评价了富含多酚和黄酮类化合物的有袋蕨(Pterocarpus marsupium, PM)心材提取物对高脂饮食(HFD)诱导的雄性Wistar大鼠动脉粥样硬化模型的保护作用。36只大鼠分为6组(n = 6),分别给予正常或HFD,加或不加阿托伐他汀或PM提取物。8周后,评估血流动力学、生化、氧化应激和炎症参数,以及主动脉组织学。饲喂hfd的大鼠心率、血脂、肝酶和丙二醛水平升高,有动脉粥样硬化的组织学征象。PM治疗显著降低甘油三酯和MDA水平,适度改善HDL水平。TNF-α和IL-6未见明显变化。组织学显示pm处理大鼠脂质浸润减少。PM提取物具有抗动脉粥样硬化和抗氧化作用,值得进一步研究其在心血管疾病中的治疗潜力。
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引用次数: 0
AMP-activated protein kinase as a therapeutic target: effects of nano-selenium and thymoquinone in Alzheimer's disease. amp活化蛋白激酶作为治疗靶点:纳米硒和百里醌在阿尔茨海默病中的作用。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-08-01 Epub Date: 2026-03-11 DOI: 10.1080/13813455.2026.2640885
Noha Amr El-Sabbagh, Doha El-Sayed Ellakwa

Context: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and complex multifactorial pathogenesis. AMP-activated protein kinase (AMPK) has been identified as a promising molecular target in AD due to its neuroprotective functions, particularly in energy regulation.

Objective: To evaluate the effects of nano-selenium and thymoquinone (TQ) on AMPK gene expression in an AD rat model.

Subjects and methods: Fifty male albino rats were divided into five groups. Four groups were induced with AD via lipopolysaccharide (LPS) injection, while the control group remained untreated. The experimental groups received nano-selenium, TQ, or a combination of both treatments. AMPK gene expression in brain tissue was measured using real-time PCR analysis.

Results: Treatment with nano-selenium, TQ, or their combination significantly upregulated AMPK expression in brain tissue compared to untreated AD rats (p<0.001). The combination therapy produced the highest increase in AMPK expression.

Discussion and conclusion: Nano-selenium and TQ enhance AMPK gene expression in AD, suggesting a potential therapeutic mechanism involving AMPK-related pathways.

背景:阿尔茨海默病(AD)是一种以进行性认知能力下降和复杂的多因素发病为特征的神经退行性疾病。amp活化蛋白激酶(AMPK)由于其神经保护功能,特别是在能量调节方面的功能,已被确定为阿尔茨海默病的一个有前途的分子靶点。目的:探讨纳米硒和百里醌(TQ)对AD模型大鼠AMPK基因表达的影响。实验对象与方法:雄性白化大鼠50只,随机分为5组。4组小鼠采用脂多糖(LPS)诱导AD,对照组不进行治疗。实验组接受纳米硒、TQ或两种治疗的组合。实时荧光定量PCR检测脑组织AMPK基因表达。结果:与未治疗的AD大鼠相比,纳米硒、TQ或它们的联合治疗显著上调了脑组织AMPK的表达(p)讨论和结论:纳米硒和TQ增强了AD中AMPK基因的表达,提示可能的治疗机制涉及AMPK相关途径。
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引用次数: 0
Polygonatum kingianum alleviates diabetic inflammation via the Mef2d/Rufy4-autophagy axis to drive macrophage M2 polarisation. 黄精通过Mef2d/ rufy4自噬轴驱动巨噬细胞M2极化减轻糖尿病炎症。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-08-01 Epub Date: 2026-01-06 DOI: 10.1080/13813455.2025.2612080
Yan Gao, Zhengfeng Liang, Shuhui Ouyang, Jingsong Cao

Chronic inflammation associated with abnormal activation of macrophages is an important promoter of type 2 diabetes (T2D) and its complications. However, there are no effective strategies for mitigating chronic inflammation. This study demonstrated that Polygonatum kingianum (P.K.) can promote macrophages M2 polarisation and increase the expression of anti-inflammatory cytokines. The mechanism involved P.K. upregulation of Mef2d expression, a key gene involved in M2 macrophage polarisation. Mef2d targeted and promoted the expression of Rufy4, thereby activating autophagy and ultimately resulting in M2 macrophage polarisation. P.K. significantly increased the number of M2 macrophages in the bone marrow and kidney while concurrently reducing the serum levels of CRP in a murine model of T2D. In summary, this study confirms that P.K. induces macrophage M2 polarisation via the Mef2d-Rufy4-autophagy pathway, which alleviates chronic inflammation associated with T2D. This study lays a foundation for the prevention and treatment of vascular complications in patients with T2D.

与巨噬细胞异常激活相关的慢性炎症是2型糖尿病(T2D)及其并发症的重要启动子。然而,目前还没有有效的策略来减轻慢性炎症。本研究表明,黄精可促进巨噬细胞M2极化,增加抗炎细胞因子的表达。其机制与P.K.上调Mef2d表达有关,Mef2d是参与M2巨噬细胞极化的关键基因。Mef2d靶向并促进Rufy4的表达,从而激活自噬,最终导致M2巨噬细胞极化。在小鼠T2D模型中,P.K.显著增加骨髓和肾脏中M2巨噬细胞的数量,同时降低血清CRP水平。综上所述,本研究证实P.K.通过mef2d - rufy4自噬途径诱导巨噬细胞M2极化,从而缓解T2D相关的慢性炎症。本研究为T2D患者血管并发症的预防和治疗奠定了基础。
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引用次数: 0
Statement of Retraction: Long non-coding RNA MEG3 and its genetic variant rs941576 are associated with rheumatoid arthritis pathogenesis in Egyptian patients. 撤回声明:长链非编码RNA MEG3及其遗传变异rs941576与埃及患者的类风湿关节炎发病有关。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-07-31 DOI: 10.1080/13813455.2026.2710002
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引用次数: 0
Trophoblast invasion dynamics improve through protein-mediated enhancement of uterine vascular remodelling pathways. 滋养细胞侵袭动力学通过蛋白质介导增强子宫血管重构途径改善。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-07-30 DOI: 10.1080/13813455.2026.2699136
Chenghong Xie, Jingqiong Zhan, Yufang Xiang

Background: In early pregnancy, trophoblast invasion and uterine vascular remodelling must be tightly regulated to ensure maternal-foetal circulation. Inhibition of these processes causes preeclampsia, foetal development retardation, and recurrent pregnancy loss. It is unclear whether molecular regulators control trophoblast invasiveness and uterine vascular adaption, despite much investigation. Methods: Here, a Protein-Mediated Vascular Remodelling Enhancement (PM-VRE) technique is proposed to examine trophoblast invasion mediated by particular regulatory proteins by increasing uterine vascular remodelling. Protein expression profiling and pathway interaction analysis comprise PM-VRE. Results: Experiments show protein signalling drives endothelial transformation, artery remodelling, and trophoblast migration, with upregulated angiogenic and matrix pathways enabling vascular adaptation. It achieves higher trophoblast invasion depths (∼195-210 µm), enhanced endothelial responsiveness (up to 95%), increased ECM remodelling activity (∼75-80), greater vascular resistance reduction (∼78%), and improved placental perfusion stability (up to 90). Conclusion: PM-VRE provides an effective framework for identifying molecular regulators of trophoblast invasion and uterine vascular remodeling, offering insights into mechanisms underlying placental development and pregnancy disorders associated with impaired placentation.

背景:在妊娠早期,滋养细胞侵袭和子宫血管重构必须严格调控,以保证母胎循环。这些过程的抑制导致先兆子痫,胎儿发育迟缓,和反复妊娠丢失。尽管进行了大量的研究,但尚不清楚分子调节剂是否控制滋养细胞的侵袭性和子宫血管的适应性。方法:本文采用蛋白质介导的血管重构增强(PM-VRE)技术,通过增强子宫血管重构来检测特定调节蛋白介导的滋养细胞侵袭。蛋白表达谱和途径相互作用分析包括PM-VRE。结果:实验表明,蛋白质信号驱动内皮转化、动脉重构和滋养细胞迁移,血管生成和基质通路的上调使血管适应。它可以达到更高的滋养细胞侵袭深度(~ 195-210µm),增强内皮反应性(高达95%),增加ECM重塑活性(~ 75-80),更大的血管阻力降低(~ 78%),改善胎盘灌注稳定性(高达90)。结论:PM-VRE为鉴定滋养细胞侵袭和子宫血管重构的分子调节因子提供了有效的框架,为胎盘发育和胎盘受损相关妊娠疾病的机制提供了见解。
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引用次数: 0
Statement of Retraction: Long non-coding RNA SNHG15 regulates cardiomyocyte apoptosis after hypoxia/reperfusion injury via modulating miR-188-5p/PTEN axis. 撤回声明:长链非编码RNA SNHG15通过调节miR-188-5p/PTEN轴调控缺氧/再灌注损伤后心肌细胞凋亡。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-07-28 DOI: 10.1080/13813455.2026.2710004
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引用次数: 0
Correction. 修正。
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-07-25 DOI: 10.1080/13813455.2026.2709942
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引用次数: 0
Physiological impact of Ba Duan Jin versus conventional breathing exercises on pulmonary function and respiratory biomarkers in chronic obstructive pulmonary disease. 八段金与常规呼吸练习对慢性阻塞性肺疾病患者肺功能和呼吸生物标志物的生理影响
IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Pub Date : 2026-07-25 DOI: 10.1080/13813455.2026.2701305
Songfeng Jin, Xuefeng Yu, Jiangtao Yin, Yujuan Guan, Dinglei Li, Xiaohuan Ding, Yinghai Cui

Background: Chronic obstructive pulmonary disease (COPD) is a common, manageable chronic respiratory disorder characterised by persistent airflow limitation. This study evaluated the effectiveness of Ba Duan Jin exercise in improving respiratory function in COPD patients.

Methods: One hundred COPD patients were randomly assigned to a Ba Duan Jin group or a control group (50 each). The Ba Duan Jin group practiced for 30 minutes, five days per week, for 12 weeks, while the control group received no exercise intervention. Outcomes including FEV1%, COPD Assessment Test (CAT), Traditional Chinese Medicine (TCM) syndrome scores, and 6-minute walk distance (6MWD) were assessed at baseline, weeks 4, 8, 12, and at 24-week follow-up.

Results: The Ba Duan Jin group showed significant improvements in lung function, exercise capacity, dyspnoea, and quality of life compared to controls, with benefits maintained at follow-up (p < 0.05-0.01).

Conclusion: Ba Duan Jin significantly improves respiratory function and quality of life in COPD patients.

背景:慢性阻塞性肺疾病(COPD)是一种常见的、可控制的慢性呼吸系统疾病,其特征是持续的气流限制。本研究评价八段劲运动对COPD患者呼吸功能的改善效果。方法:100例慢性阻塞性肺病患者随机分为八段金组和对照组各50例。八段金组每周练习5天,每次30分钟,持续12周,而对照组没有任何运动干预。在基线、第4周、第8周、第12周和第24周随访时评估FEV1%、COPD评估测试(CAT)、中医(TCM)证型评分和6分钟步行距离(6MWD)。结果:与对照组相比,八段金组在肺功能、运动能力、呼吸困难和生活质量方面均有显著改善,且在随访中获益保持(p)。结论:八段金可显著改善COPD患者的呼吸功能和生活质量。
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引用次数: 0
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Archives of Physiology and Biochemistry
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