Biomedicine & Pharmacotherapy最新文献_第7页

Activation of SIK1 in the paraventricular nucleus by phanginin A induces antidepressant-like actions in male mice via suppressing hyperactivity of the hypothalamus-pituitary-adrenal axis phanginin A激活室旁核SIK1，通过抑制下丘脑-垂体-肾上腺轴的过度活跃，在雄性小鼠中诱导抗抑郁样作用。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118979

Chao Liu , Xue-Yan Zhu , Jia-Jia Shi , Fei Jiang , Xiang-Ming Cai , Yan-Ni Shi , Qi Yan , Bo Jiang , Hua Fan , Lei Ji , Pei-Juan Wang

Background

Current monoaminergic antidepressants demonstrate limited efficacy and delayed onset, necessitating novel treatment strategies. Previous studies have identified salt-inducible kinase 1 (SIK1) in the paraventricular nucleus (PVN) as an important regulator of depression pathogenesis by controlling nuclear translocation of cAMP response element-binding protein (CREB)-regulated transcription coactivator 1 (CRTC1) and activity of the hypothalamus-pituitary-adrenal (HPA) axis. The current study investigated the antidepressant-like efficacy of phanginin A, a newly discovered potent SIK1 activator, in male C57BL/6 J mice.

Methods

Two well-validated depression models (chronic social defeat stress and chronic unpredictable mild stress) were established to examine the efficacy of phanginin A treatment against chronic stress-induced HPA hyperactivity and depression-like behaviors including desperate mood, anhedonia, and social avoidance. Western blotting, immunofluorescence, and co-immunoprecipitation were then conducted to evaluate the biological changes in not only the SIK1-CRTC1 signaling in PVN neurons but also the hippocampal brain derived neurotrophic factor (BDNF) signaling and adult neurogenesis among all groups. To further determine the antidepressant mechanism of phanginin A, model mice were re-examined following genetic knockdown of SIK1 in the PVN.

Results

Phanginin A administration suppressed depression-like behaviors in both models, normalized chronic stress-induced alteration in the SIK1-CRTC1 signaling in PVN neurons, and rescued chronic stress-induced impairments in hippocampal BDNF signaling and adult neurogenesis. Knockdown of SIK1 in the PVN abrogated the antidepressant-like actions of Phanginin A in male mice.

Conclusion

Our findings further establish SIK1 in the PVN as an antidepressant target and support phanginin A as a potential antidepressant candidate.

背景：目前的单胺类抗抑郁药疗效有限且起效延迟，需要新的治疗策略。先前的研究发现，室旁核（PVN）中的盐诱导激酶1 （SIK1）通过控制cAMP反应元件结合蛋白（CREB）调控的转录辅激活因子1 （CRTC1）的核易位和下丘脑-垂体-肾上腺（HPA）轴的活性，成为抑郁症发病的重要调节因子。本研究在雄性C57BL/6 J小鼠中研究了phanginin A（一种新发现的强效SIK1激活剂）的抗抑郁样功效。方法：建立两种有效的抑郁症模型（慢性社会失败应激和慢性不可预测的轻度应激），观察苯甲素A治疗慢性应激性HPA亢进和抑郁样行为（绝望情绪、快感缺乏和社交回避）的疗效。采用Western blotting、免疫荧光、共免疫沉淀等方法观察各组PVN神经元SIK1-CRTC1信号通路、海马脑源性神经营养因子（BDNF）信号通路和成体神经发生的生物学变化。为了进一步确定phanginin A的抗抑郁机制，我们在PVN中基因敲低SIK1后对模型小鼠进行了重新检测。结果：Phanginin A抑制了两种模型的抑郁样行为，使PVN神经元中SIK1-CRTC1信号通路的慢性应激诱导改变正常化，并挽救了海马BDNF信号通路和成人神经发生的慢性应激诱导损伤。在雄性小鼠中，PVN中SIK1的敲低消除了Phanginin A的抗抑郁样作用。结论：我们的研究结果进一步证实了PVN中的SIK1是一个抗抑郁靶点，并支持了phanginin A作为一个潜在的抗抑郁候选药物。

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引用次数: 0

GLP-1 receptor activation and neuroprotection: Bridging the gap between metabolic signaling and structural preservation via the cAMP/CREB axis GLP-1受体激活和神经保护：通过cAMP/CREB轴弥合代谢信号和结构保存之间的差距。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118977

Chien-Wei Huang, Su-Boon Yong, Chia-Jung Li

引用次数: 0

As a novel ferroptosis inhibitor, primaquine alleviates I/R-induced retinal neuron death via increasing GSTA1 activity 作为一种新型的铁下垂抑制剂，伯氨喹通过增加GSTA1活性来减轻I/ r诱导的视网膜神经元死亡。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118973

Shuang Lu , Lewen Wang , Keting Wang , Kun Xiong , Weitao Yan

Ischemia-reperfusion (I/R)-induced retinal ganglion cells (RGCs) death involves multiple types of regulated cell death. Ferroptosis plays an active role in retinal I/R injury. Primaquine, a classical antimalarial drug, has unique pharmacological properties that suggest it may inhibit ferroptosis. We employed an acute high intraocular pressure (aHIOP) mouse model and oxygen-glucose deprivation/reoxygenation (OGD/R) injury in R28 cells to investigate the effects of primaquine on retinal I/R injury. Transcriptomic sequencing at both the animal and cellular levels identified glutathione S-transferase alpha 1 (GSTA1) as a potential key target of primaquine. In vitro, primaquine treatment inhibited cell death induced by OGD/R, Erastin, and RSL3. It suppressed the accumulation of ROS and Fe²⁺, ameliorated mitochondrial morphological damage, and promoted the increased expression of SLC7A11 and GPX4. Primaquine administration reduced RGC layer cell loss, increased retinal thickness, and upregulated SLC7A11 and GPX4 protein levels in the retina. Knocking down GSTA1 expression reversed the protective effects of primaquine against ferroptosis induced by OGD/R, Erastin, or RSL3. Our study offers new insights into the critical function of primaquine in inhibiting ferroptosis via modulating GSTA1 activity in retinal neuron induced by OGD/R, Erastin, or RSL3, a mechanism that has not been previously explored.

缺血再灌注（I/R）诱导的视网膜神经节细胞（RGCs）死亡涉及多种类型的调节细胞死亡。上睑下垂在视网膜I/R损伤中起积极作用。伯氨喹是一种经典的抗疟疾药物，具有独特的药理特性，表明它可能抑制铁下垂。我们采用急性高眼压（aHIOP）小鼠模型和R28细胞氧-葡萄糖剥夺/再氧化（OGD/R）损伤来研究伯氨喹对视网膜I/R损伤的影响。动物和细胞水平的转录组测序鉴定谷胱甘肽s -转移酶α 1 （GSTA1）是伯氨喹的潜在关键靶点。在体外，伯氨喹可抑制OGD/R、Erastin和RSL3诱导的细胞死亡。抑制ROS和Fe 2 +的积累，改善线粒体形态损伤，促进SLC7A11和GPX4的表达增加。伯氨喹可减少RGC层细胞损失，增加视网膜厚度，上调视网膜中SLC7A11和GPX4蛋白水平。抑制GSTA1表达逆转了伯氨喹对OGD/R、Erastin或RSL3诱导的铁死亡的保护作用。我们的研究为伯氨喹通过调节OGD/R、Erastin或RSL3诱导的视网膜神经元中GSTA1活性来抑制铁凋亡的关键功能提供了新的见解，这一机制以前没有被探索过。

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引用次数: 0

Neuroendocrine signaling as a pathological seed for the female bias of Alzheimer’s disease and the concept of estrobolome 神经内分泌信号作为阿尔茨海默病女性偏倚的病理种子和雌激素的概念。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118999

Deepthi Rapaka , Arthur Saniotis , Monkgogi Thatayaone , Veera Raghavulu Bitra

The prevalence of Alzheimer's disease (AD) is anticipated to escalate with the global increase in life expectancy. Although sex-based differences in AD have been previously documented, doubts persist regarding the relationship between sex and pathophysiological pathways. Sex hormones may contribute to these disparities, with a heightened risk of AD-related dementia associated with oophorectomy before menopause. We cannot ascertain if estrogens alone are solely accountable for this accelerated pathological progression of the disease. Estrogens are regulated by the gut microbiota. Thus, the gut-estrogen-brain axis appears to be implicated as a potential new influencer in the pathophysiology of AD, as the female microbiome differs from the male gut microbiome. This suggests it could be a risk factor for the higher prevalence of AD in women. This review speculates on the possible mechanisms for AD prevalence in women, including both anatomical and neuroendocrinological perspectives.

随着全球预期寿命的增加，阿尔茨海默病（AD）的患病率预计将逐步上升。尽管先前有文献记载了阿尔茨海默病的性别差异，但性别与病理生理途径之间的关系仍然存在疑问。性激素可能是造成这些差异的原因之一，绝经前进行卵巢切除术会增加ad相关痴呆的风险。我们不能确定是否雌激素单独负责这种疾病的加速病理进展。雌激素是由肠道菌群调节的。因此，肠道-雌激素-脑轴似乎与阿尔茨海默病病理生理的潜在新影响有关，因为女性肠道微生物组不同于男性肠道微生物组。这表明它可能是女性AD患病率较高的一个风险因素。本文从解剖学和神经内分泌学两方面对女性AD患病率的可能机制进行了推测。

引用次数: 0

Liver kinome reveals PS1145 as therapeutic agent for mitigating systemic inflammation in alcohol-related liver disease 肝脏kinome显示PS1145可作为缓解酒精相关性肝病全身性炎症的治疗剂。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118984

Manisha Yadav , Abhishak Gupta , Sanju Yadav , Vipul Sharma , Yash Magar , Deepanshu Deepanshu , Tahseen Khan , Neha Sharma , Kavita Yadav , Nupur Sharma , Vasundhra Bindal , Sushmita Pandey , Gaurav Tripathi , Rimsha Saif , Babu Mathew , Dinesh Mani Tripathi , Anupama Kumari , Shvetank Sharma , Shiv Kumar Sarin , Jaswinder Singh Maras

Rationale

Alcohol-related liver disease (ALD) lacks effective anti-inflammatory therapies, and since kinases orchestrate inflammation, kinome profiling offers a rational approach to identify and validate novel therapeutic targets.

Objective

To analyse liver and monocyte kinome alterations in a chronic ethanol-fed pre-clinical rat model and identify therapeutic targets capable of mitigating inflammation. Pathway-specific inhibitors, including PS1145 (IKK-phosphorylation-inhibitor), PH797804 (MAPK14-inhibitor), resveratrol, and prednisolone were evaluated in ALD-rats, PBMCs from patients, and the NIAAA mouse model.

Findings

Kinome profiling identified 497 hepatic and 345 monocyte kinases in ALD rats (FDR<0.01), with a time-dependent increase in MAPK14-associated kinases in both tissues (FC>1.5, p < 0.05). By 24 weeks, 172-liver and 48-monocyte kinases were upregulated, primarily involving MyD88-TLR4, PI3K-Akt, TNF, TGFβ-TGFβR1, senescence and ROS-generating kinases and IL-1-driven MAPK14 and IKK phosphorylation(p < 0.05). Targeting this axis, PS1145 suppressed NFκB activation and inflammation in THP1, HepG2 cells, PBMCs from healthy and SAH-patients, outperforming PH797804, resveratrol, and prednisolone (FC>1.5,p < 0.05). PS1145 significantly reduced IL-6, TNFα, and NFκB, while increasing IL-10. In NIAAA-mouse model, PS1145 treatment reduced hepatic steatosis, cellular stress, and inflammation, IL36R disrupting TLR dimerization more effectively than standard therapies (p < 0.05).

Conclusion

PS1145 blocks IKK phosphorylation and TLR dimerization, attenuating inflammation and improving liver pathology, highlighting its therapeutic potential in ALD.

理由：酒精相关性肝病（ALD）缺乏有效的抗炎治疗，由于激酶调控炎症，因此kinome谱分析提供了一种合理的方法来识别和验证新的治疗靶点。目的：分析慢性乙醇喂养的临床前大鼠模型肝脏和单核细胞激酶的变化，并确定能够减轻炎症的治疗靶点。途径特异性抑制剂，包括PS1145 （ikk -磷酸化抑制剂）、PH797804 （mapk14抑制剂）、白藜芦醇和强的松龙在ald大鼠、患者PBMCs和NIAAA小鼠模型中进行了评估。研究结果：在ALD大鼠中，通过Kinome分析鉴定出497个肝脏激酶和345个单核细胞激酶（FDR1.5, p 1.5,p ）。结论：PS1145阻断IKK磷酸化和TLR二聚化，减轻炎症，改善肝脏病理，突出其治疗ALD的潜力。

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引用次数: 0

Comparative analysis of nicotine dynamics and antioxidant enzyme activity in high-tar and low-tar tobacco combustion users and healthy volunteers 高焦油和低焦油烟草燃烧使用者与健康志愿者尼古丁动态和抗氧化酶活性的比较分析。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118987

Sudarshan Parameswaran , Shakthi Rajaraman , Deepika Ravi Sankar , Jeevadharsana Gowthaman , Premkumar Kumar , Raman Lakshmi Sundaram , Jerad A. Suresh , Balamurugan Sivakumar , Gayathri Thiruvengadam , Murugesan Arumugam

This study investigated the influence of smoking exposure and reported cigarette type on antioxidant enzyme activity and nicotine and cotinine profiles in smokers. Participants were classified as low-tar (LT, n = 23) or high-tar (HT, n = 21) smokers based on self-reported cigarette type, and these reports were further confirmed using expired CO levels. A control group of non-smokers (n = 28) was also selected based on expired CO measurements for comparison. Plasma nicotine and cotinine concentrations were quantified using HPLC before and after incubation with ascorbic acid, whereas superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase-1 (GPx-1) activities were determined using ELISA. LT smokers exhibited significantly reduced CAT activity (p = 0.0021) and a modest, non-significant increase in the nicotine-to-cotinine (NC) ratio after incubation. In HT smokers, the post-incubation NC ratio correlated positively with oxidative stress markers, including the R ratio (r = 0.571, p = 0.007), SC ratio (r = 0.611, p = 0.004), and SOD activity (r = 0.592, p = 0.006). These findings suggest that differences in smoke exposure and reported cigarette type are associated with variations in redox-related measures under the experimental conditions studied.

本研究调查了吸烟暴露和卷烟类型对吸烟者抗氧化酶活性以及尼古丁和可替宁谱的影响。参与者根据自我报告的香烟类型被分为低焦油（LT, n = 23）或高焦油（HT, n = 21）吸烟者，这些报告通过过期CO水平进一步得到证实。根据过期CO测量值选择非吸烟者对照组（n = 28）进行比较。采用高效液相色谱法测定抗坏血酸孵育前后血浆尼古丁和可替宁浓度，ELISA法测定超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶-1 （GPx-1）活性。LT吸烟者的CAT活性显著降低（p = 0.0021），孵育后尼古丁与可替宁（NC）比值略有增加，但不显著。在HT吸烟者,post-incubation数控比例将积极与氧化应激标记,包括R比率(R = 0.571,p = 0.007),SC比(R = 0.611,p = 0.004),和SOD活性(R = 0.592,p = 0.006)。这些发现表明，在所研究的实验条件下，烟雾暴露和报告的卷烟类型的差异与氧化还原相关测量的变化有关。

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引用次数: 0

Sex-specific characterization of a novel metabolic osteoporosis phenotype induced by NOS-inhibition and Western diet in Wistar rats nos抑制和西方饮食诱导Wistar大鼠新型代谢性骨质疏松症表型的性别特异性表征。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118989

Simon Kloock , Palina Zytner , Tom Lunkwitz , Niklas Geiger , Vasco Sequeira , Christoph Maack , Max Kurlbaum , Humma Sarwar , Anita Ignatius , Martin Fassnacht , Melanie Haffner-Luntzer , Ulrich Dischinger

Background

Multiple aspects of the metabolic syndrome are linked to impaired bone health, yet most animal models address only single contributing factors. Here, a male and female “two-hit” rat model of metabolic osteoporosis combining a high-fat/high-fructose “Western” diet (WD) and N(ω)-nitro-L-arginine-methyl-ester (L-NAME) is introduced and characterized.

Methods

Female Wistar rats were randomized into three groups: [i] Chow, [ii] Chow+L-NAME, and [iii] WD+L-NAME. Groups [i] and [iii] were replicated in males. After 16 weeks, femora were analyzed by micro-computed tomography, histology, and RNA-sequencing. Serum analyses included bone turnover markers and steroid hormones (LC/MS-MS).

Results

WD+L-NAME induced bone loss in both sexes, e.g. with the bone-volume-to-tissue-volume-ratio (BV/TV) being significantly reduced in females ([i] 53.8 ± 2.0, [iii] 43.0 ± 2.0; p < 0.01) and males ([i] 33.8 ± 7.4, [iii] 18.5 ± 9.4; p < 0.05). Female Chow+L-NAME rats exhibited elevated osteoclast numbers per bone surface ([i] 4.0 ± 1.8, [ii] 9.9 ± 3.6; p < 0.05), while no such changes occurred in WD+L-NAME females ([iii] 4.2 ± 2.7; n.s.). The Wnt-inhibitor sclerostin was significantly elevated in males on WD+L-NAME ([i] 278 ± 133, [iii] 931 ± 454 pg/ml; p < 0.05). While steroid hormones were not significantly altered, RNA-sequencing revealed a downregulation of bone formation–related pathways in both sexes under WD+L-NAME, with extracellular matrix–related gene terms being primarily affected by WD.

Conclusion

The combination of WD+L-NAME induces a metabolic osteoporosis phenotype in male and female rats. It is thereby representing the first “two-hit” model for metabolic osteoporosis with a phenotype in both sexes. Elevated DKK1 and sclerostin in males suggest Wnt-signalling involvement, while WD predominantly impacts extracellular matrix regulation.

背景：代谢综合征的多个方面与骨骼健康受损有关，但大多数动物模型只涉及单一的影响因素。本文介绍了一种采用高脂肪/高果糖“西方”饮食（WD）和N(ω)-硝基- l-精氨酸-甲酯（L-NAME）联合治疗的雄性和雌性代谢性骨质疏松大鼠模型。方法：雌性Wistar大鼠随机分为[i] Chow、[ii] Chow+L-NAME、[iii] WD+L-NAME三组。组[i]和组[iii]在雄性中重复。16周后，通过显微计算机断层扫描、组织学和rna测序对股骨进行分析。血清分析包括骨转换标志物和类固醇激素（LC/MS-MS）。结果：WD+L-NAME可诱导两性骨质流失，雌性骨体积与组织体积比（BV/TV）明显降低（[i] 53.8 ± 2.0,[iii] 43.0 ± 2.0;p ）结论：WD+L-NAME可诱导雌雄大鼠代谢性骨质疏松表型。因此，它代表了第一个具有两性表型的代谢性骨质疏松症的“双重打击”模型。男性DKK1和硬化蛋白升高提示wnt信号参与，而WD主要影响细胞外基质调节。

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引用次数: 0

Peroxisome proliferator-activated receptors in kidney diseases: A promising therapeutic target 肾脏疾病中的过氧化物酶体增殖物激活受体：一个有前途的治疗靶点。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118983

Qiuyi Li , Zhenwei Shi , Xiujie Shi , Hang Xing , Yu Zhang , Shougang Zhuang , Meiying Chang

Peroxisome proliferator-activated receptors (PPARs) play critical roles in metabolic regulation, inflammation, and cellular differentiation. Recent studies have revealed their significant involvement in a spectrum of kidney diseases, including chronic kidney disease (CKD), acute kidney injury (AKI), diabetic kidney disease (DKD), renal cell carcinoma, lupus nephritis, and autosomal dominant polycystic kidney disease. In this narrative review, we summarize current insights into the roles and mechanisms of PPARs in kidney pathophysiology and evaluate the efficacy of PPAR-targeted therapies in both animal models and clinical studies. Collectively, our analysis highlights the therapeutic potential of PPARs as promising molecular targets for renal disorders, particularly CKD, AKI, and DKD. However, important challenges remain for clinical translation, including dose-dependent adverse effects and the lack of renal-specific drug delivery, both of which highlight the need for safer and more targeted PPAR modulators.

过氧化物酶体增殖物激活受体（PPARs）在代谢调节、炎症和细胞分化中起着关键作用。最近的研究表明，它们在一系列肾脏疾病中有重要的作用，包括慢性肾病（CKD）、急性肾损伤（AKI）、糖尿病肾病（DKD）、肾细胞癌、狼疮肾炎和常染色体显性多囊肾病。在这篇叙述性综述中，我们总结了ppar在肾脏病理生理中的作用和机制，并在动物模型和临床研究中评估了ppar靶向治疗的疗效。总的来说，我们的分析强调了ppar作为肾脏疾病，特别是CKD， AKI和DKD的有希望的分子靶点的治疗潜力。然而，临床转化仍然面临重大挑战，包括剂量依赖性不良反应和缺乏肾特异性药物递送，这两者都强调需要更安全、更有针对性的PPAR调节剂。

引用次数: 0

Current status and perspective of off-the-shelf CAR-T cells in cancer immunotherapy 现成CAR-T细胞在癌症免疫治疗中的现状与展望

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118986

Shiva Fallahianshafiei , Ali Babaeizad , Piao Yang , Anita S. La'ah , Mohsen Sheykhhasan

Recent advances in cancer immunotherapy have highlighted the promise of off-the-shelf chimeric antigen receptor (CAR)-T cell therapy. This has offered solutions to key limitations of conventional autologous approaches, such as patient-specific cell collection and lengthy production times. This review summarizes the development, clinical application, and challenges of CAR-T cell technology. We reviewed CAR design and function, cancer-targeting mechanisms, and approaches to developing universal donor platforms that could replace the need for patient-specific cell harvesting. We discussed key challenges of CAR-T technology and its potential solutions. This review also summarizes CAR-T cell therapies recently approved by the FDA. Finally, we explored future directions, regulatory challenges and the potential of personalized medicine, emphasizing how off-the-shelf CAR-T therapies could revolutionize cancer treatment by making it more scalable and accessible.

癌症免疫治疗的最新进展突出了现成的嵌合抗原受体(CAR)-T细胞治疗的前景。这为传统自体方法的关键局限性提供了解决方案，例如患者特异性细胞收集和冗长的生产时间。本文综述了CAR-T细胞技术的发展、临床应用和挑战。我们回顾了CAR的设计和功能，癌症靶向机制，以及开发通用供体平台的方法，这些平台可以取代对患者特异性细胞采集的需求。我们讨论了CAR-T技术的主要挑战及其潜在的解决方案。本综述还总结了最近FDA批准的CAR-T细胞疗法。最后，我们探讨了未来的方向、监管挑战和个性化医疗的潜力，强调了现成的CAR-T疗法如何通过使其更易于扩展和获取来彻底改变癌症治疗。

引用次数: 0

Antibacterial potential of rutin nanoformulations: Current insights and future directions 芦丁纳米配方的抗菌潜力：目前的见解和未来的方向。

IF 7.5 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Biomedicine & Pharmacotherapy

Pub Date : 2026-01-12 DOI: 10.1016/j.biopha.2026.118980

Solmaz Maleki Dizaj , Saba Tohidi , Sara Salatin , Elham Ahmadian , Zoleikha Asadi , Mohammad Yousef Memar , Yasin Bagheri , Simin Sharifi

Rutin, a plant-derived flavonoid, exhibits broad pharmacological activities, including antibacterial effects against Gram-positive and Gram-negative bacteria. However, its clinical and industrial applications are restricted by poor aqueous solubility, low bioavailability, and instability under physiological conditions. To address these limitations, several nanoformulation strategies have been developed, including polymeric nanoparticles, lipid-based carriers, nanoemulsions, and micro- and nano-encapsulation techniques. These approaches have been shown to improve rutin’s solubility, dispersibility, colloidal stability, and antibacterial potency in experimental studies. Nanoformulation strategies improve solubility, stability, and controlled release, but most findings remain preclinical, with limited in vivo validation and insufficient knowledge regarding industrial-scale manufacturing. This review consolidates current data on rutin nanoformulations, emphasizing their antibacterial activity and physicochemical improvements, while also identifying key limitations that must be addressed before clinical translation.

芦丁是一种植物衍生的类黄酮，具有广泛的药理活性，包括对革兰氏阳性和革兰氏阴性细菌的抗菌作用。然而，其水溶性差，生物利用度低，生理条件下不稳定，限制了其临床和工业应用。为了解决这些限制，已经开发了几种纳米配方策略，包括聚合纳米颗粒、脂基载体、纳米乳液以及微纳米封装技术。实验研究表明，这些方法可以改善芦丁的溶解度、分散性、胶体稳定性和抗菌效力。纳米制剂策略提高了溶解度、稳定性和控释，但大多数研究结果仍处于临床前阶段，体内验证有限，对工业规模生产的了解不足。这篇综述整合了目前关于芦丁纳米制剂的数据，强调了它们的抗菌活性和物理化学改进，同时也确定了在临床转化之前必须解决的关键限制。

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引用次数: 0