FOOD RESEARCH INTERNATIONAL
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2026
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IF 8.8
Yueqin Qiu,Shilong Liu,Xinmiao Liao,Wenjing Wang,Jiaxi Tang,Li Wang,Xuefen Yang,Zongyong Jiang
Geniposide alleviated intestinal barrier dysfunction. • Geniposide increased Prevotella copri abundance to alleviate intestinal injury. • Geniposide inhibited diquat-induced intestinal ferroptosis in vivo and in vitro . • Geniposide regulated TRPV4/GPX4-mediated ferroptosis to alleviated intestinal injury. Early weaning disrupts intestinal antioxidant capacity and barrier integrity in human infants and young animals. Geniposide, an iridoid glycoside, exhibits anti-inflammatory and antioxidant activities. However, the mechanism by which geniposide ameliorates weaning-associated intestinal oxidative injury remains to be elucidated. Therefore, this study aimed to investigate whether and how geniposide attenuates intestinal injury, using diquat (DQ)-challenged weaned piglets, mice, and IPEC-J2 cells as experimental models. The results showed that geniposide supplementation significantly alleviated DQ-induced growth inhibition by increasing ADG and ADFI in the piglets. Additionally, geniposide significantly alleviated DQ-induced intestinal barrier damage, as evidenced by increased gene and protein expression of occludin and claudin-1 and decreased intestinal permeability in the ileum. Moreover, geniposide significantly attenuated DQ-induced oxidative stress, as shown by reduced levels of MDA, ROS, and 4-HNE, along with increased activities of T-AOC, GSH-Px, and T-SOD, as well as upregulated protein abundance of NRF2 and GCLM. Microbiome analysis showed that geniposide significantly increased Prevotella copri abundance in the ileum of DQ-challenged piglets. Prevotella copri supplementation alleviated DQ-induced intestinal injury in mice. Transcriptomic and non-targeted metabolomic analyses revealed that geniposide inhibited the DQ-induced ferroptosis signaling pathway. Additionally, geniposide significantly alleviated the DQ-induced the increases in the levels of MDA and Fe 2+ , and restored expression of the anti-ferroptotic proteins GPX4, SLC7A11, and FTL. Mechanistically, geniposide inhibited DQ-induced intestinal ferroptosis through modulation of the TRPV4/GPX4 pathway and increasing Prevotella copri abundance. Collectively, this study revealed that geniposide alleviated DQ-induced intestinal injury by modulating the TRPV4/GPX4-mediated ferroptosis pathway and increasing Prevotella copri abundance, suggesting its potential as a therapeutic agent against weaning-associated intestinal oxidative damage. Download: Download high-res image (117KB) Download: Download full-size image
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DOI
高影响因子
JOURNAL OF PHARMACEUTICAL SCIENCES
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2025
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IF 3.8
Tianyu He,Rong Tian,Zhichao Song,Lei Liu,Xixi Zhu,Yanan Li,Wenjun Liu,Shaoping Yin,Jie Dong,Fei Xu,Jun Chen
Natural terpenes found in essential oils (EOs) have shown promise as penetration enhancers (PEs) in pharmaceutical and cosmetic formulations. This study compared the skin penetration enhancement properties of sesquiterpenes and monoterpenes from galangal EO (GEO), e.g. δ-cadinene, β-caryophyllene, caryophyllene oxide (CPO), 4-terpineol, β-pinene, and 1,8-cineole. Results indicated that the sesquiterpenes, particularly δ-cadinene, significantly improved the skin permeation of rhodamine B compared to monoterpenes. Electrical resistance measurements of the skin, DSC and XRD analysis revealed that the sesquiterpenes notably disturbed the ordered arrangement of stratum corneum (SC) components including lipids and keratins. Additionally, the results of molecular docking also revealed that sesquiterpenes were easily combined with transient receptor potential vanilloid 4 (TRPV4) ion channel. The cutaneous TRPV4 ion channel, which played a role in tight junction (TJ) formation in keratinocytes, were abundantly expressed in rat abdominal skin. δ-Cadinene, specifically, exhibited an agonistic effect on the cutaneous TRPV4 ion channel, significantly enhancing its SC retention and facilitating in vivo skin permeation of rhodamine B. In summary, the penetration enhancement mechanism of sesquiterpenes from GEO, particularly δ-cadinene, includes acting on SC components and activating the cutaneous TRPV4 ion channel.
研究领域:
药学科学
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皮肤科学
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天然产物化学
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透皮药物递送
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分子药理学
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产品关联
DOI
PubMed
高影响因子
Cell Metabolism
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2025
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IF 30.9
Tingting Zhou,Zhiwei Wang,Xiaowang Lv,Mengting Guo,Ning Zhang,Liangju Liu,Li Geng,Jing Shao,Ka Zhang,Mengru Gao,Aiqin Mao,Yifei Zhu,Fan Yu,Lei Feng,Xiaoyan Wang,Qixiao Zhai,Wei Chen,Xin Ma
Currently, the regulation of specific gut microbial metabolism for the development and/or treatment of hypertension remains largely unexplored. Here, we show that α-lipomycin, produced by Streptomyces aureofaciens ( S. aureofaciens ) Tü117, is upregulated in the serum of high-salt diet (HSD) mice and patients with essential hypertension. α-lipomycin causes vasodilation impairment involving transient receptor potential vanilloid 4 (TRPV4)-mediated nitric oxide and endothelium-derived hyperpolarizing factor pathways in mice. We also find that Lactobacillus plantarum ( L. plantarum ) CCFM639 attenuates the increase in blood pressure (BP) potentially through inhibiting the proliferation of S. aureofaciens Tü117 in mice. An exploratory intervention trial indicates that L. plantarum CCFM639 supplementation reduces BPs in subjects newly diagnosed with pre-hypertension or stage 1 hypertension without antihypertensive medication. Our findings provide evidence for a role of S. aureofaciens Tü117-associated α-lipomycin elevation in the pathogenesis of HSD-induced hypertension, highlighting that targeting gut bacteria serves as a new therapeutic intervention for hypertension.
研究领域:
微生物学
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药理学
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心血管疾病
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产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
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2022
·Vol. 12
·期 3
·2201925
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IF 11.092
Xianpeng Huang,Di Chen,Chengzhen Liang,Kesi Shi,Xiaopeng Zhou,Yuang Zhang,Yi Li,Jiangjie Chen,Kaishun Xia,Jiawei Shu,Biao Yang,Jingkai Wang,Haibin Xu,Chao Yu,Feng Cheng,Shaoke Wang,Yongxiang Zhang,Chenggui Wang,Liwei Ying,Hao Li,Meiling Han,Fangcai Li,Yiqing Tao,Qian Zhao,Qixin Chen
Mechanical stimulation is an effective approach for controlling stem cell differentiation in tissue engineering. However, its realization in in vivo tissue repair remains challenging since this type of stimulation can hardly be applied to injectable seeding systems. Here, it is presented that swelling of injectable microgels can be transformed to in situ mechanical stimulation via stretching the cells adhered on their surface. Poly(acrylamide- co -acrylic acid) microgels with the upper critical solution temperature property are fabricated using inverse emulsion polymerization and further coated with polydopamine to increase cell adhesion. Adipose-derived mesenchymal stem cells (ADSCs) adhered on the microgels can be omnidirectionally stretched along with the responsive swelling of the microgels, which upregulate TRPV4 and Piezo1 channel proteins and enhance nucleus pulposus (NP)-like differentiation of ADSCs. In vivo experiments reveal that the disc height and extracellular matrix content of NP are promoted after the implantation with the microgels. The findings indicate that swelling-induced mechanical stimulation has great potential for regulating stem cell differentiation during intervertebral disc repair.
研究领域:
组织工程
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干细胞生物学
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生物医学工程
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骨科
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产品关联
DOI
PubMed
高影响因子
ADVANCED FUNCTIONAL MATERIALS
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2025
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IF 19
Xiaoyang Wu,Shiji Lu,Yusheng Zhang,Kai Wu,Junzhong Jiang,Xiaoyin Liu,Dan Wei,Chengheng Wu,Jie Ding,Liangxue Zhou,Jing Sun,Hongsong Fan
Ischemic stroke induces catastrophic neurovascular damage through hypoxia- driven neuronal death and metabolic collapse, characterized by Adenosine Triphosphate (ATP) depletion and mitochondrial dysfunction. In this work, an injectable granular hydrogel platform GUD-HB@PDA is developed, composed of ureidopyrimidinone/dopamine (UPy/DA)-functionalized gelatin (GUD) microspheres and polydopamine-coated hemoglobin (HB@PDA). Attributing to UPy-based quadruple hydrogen bonding and catechol-mediated crosslinking, the hydrogel platform achieves brain-mimetic dynamic viscoelasticity and sustained oxygenation delivery. The import role of viscoelasticity and oxygen supplementation in energy metabolism regulation is confirmed. Notably, it is found that the oxygen supplementation contributes 36–39% ATP increase through alleviates hypoxia, while viscoelastic mechanics contributes 61–64% of ATP increase, dominating the energy regulation through TRPV4-mediated mechanotransduction. This study proves this mechanical bioenergetic regulation synergizing with oxygen-dependent pathways promotes neuronal differentiation and angiogenesis in ischemic-hypoxic environment, through concurrent activation of AMPK-mTOR metabolic pathways and neurogenic differentiation programs. In a photothrombotic stroke model, superior therapeutic efficacy with 5.4-fold neuronal maturation, 1.6-fold vascular infiltration, and 2.8-fold axonal regeneration versus present reports are demonstrated. In summary, focusing on mechanical mismatch and bioenergetic deficits, a unique strategy of viscoelasticity-oxygenation synergy through mechanical cues as fundamental metabolic regulators is established, providing a robust solution for energy-intensive neurovascular regeneration following ischemic stroke.
研究领域:
生物材料
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神经工程
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组织工程
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卒中治疗
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机械生物学
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生物能量学
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产品关联
DOI
高影响因子
Acta Biomaterialia
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2025
·
IF 9.6
Yuanqi Chen,Kezheng Lei,Yinxi Li,Zhixiang Mu,Tengda Chu,Jiajun Hu,Bairui Zeng,Yi Wang,Jianliang Shen,Xiaojun Cai,Tianpeng Shi,Hui Deng
Oral mucosal wounds are more prone to inflammation due to direct exposure to various microorganisms. This can result in pain, delayed healing, and other complications, affecting patients' daily activities such as eating and speaking. Consequently, the overall quality of life for patients is significantly reduced. To address these challenges, we developed a multifunctional therapeutic nanoplatform, DATS@Arg-EA-SA, through the self-assembly of guanidinated dendritic peptides (Arg-EA-SA) that encapsulate diallyl trisulfide (DATS), a hydrogen sulfide (H 2 S) donor. The guanidine-rich surface of DATS@Arg-EA-SA efficiently neutralizes reactive oxygen species (ROS) in the ulcer microenvironment, generating nitric oxide (NO), which acts as the primary antimicrobial agent by disrupting bacterial membranes. Concurrently, the presence of glutathione triggers the release of H 2 S from DATS, providing supplementary antibacterial support. DATS@Arg-EA-SA effectively kills all bacteria, achieving results comparable to those of penicillin, a classical antibiotic. Moreover, it demonstrates superior sterilization efficacy against drug-resistant bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA), significantly outperforming penicillin. Following the initial antimicrobial phase, the nanoplatform transitions into an anti-inflammatory stage. H 2 S, in synergy with NO, facilitates the conversion of M1 macrophages to M2 macrophages, thereby reducing the expression of inflammatory factors. Importantly, the combination of H 2 S and NO provides effective analgesia by downregulating the expression of TRPV1 and TRPV4, thus restoring normal dietary behaviors and improving the overall quality of life. This system ultimately promotes collagen fiber deposition and accelerates the re-epithelialization of the ulcer wound, positioning DATS@Arg-EA-SA as a promising gas-delivery nanoplatform for rapid wound repair in the clinical treatment. Statement of Significance Oral mucosal wounds are highly susceptible to microbial infections, leading to inflammation, pain, delayed healing, and a significant decline in quality of life. We developed a multifunctional therapeutic nanoplatform (DATS@Arg-EA-SA) via the self-assembly of guanidinated dendritic peptides encapsulating the H 2 S donor DATS, which exhibited antibacterial, anti-inflammatory, and analgesic properties. In the oral ulcer microenvironment, DATS@Arg-EA-SA generates substantial NO under elevated ROS levels, while glutathione triggers the controlled release of H 2 S. NO disrupts bacterial membranes as the primary antibacterial agent, with H 2 S providing synergistic antibacterial effects. Furthermore, H 2 S and NO synergistically promote the transformation of M1 to M2 macrophages, attenuating inflammation. Importantly, the combined action of H 2 S and NO alleviates pain by downregulating TRPV1 and TRPV4, supporting the restoration of normal dietary behavior and improving quality of life.
研究领域:
药学
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纳米技术
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生物材料
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医学
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牙科
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炎症研究
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伤口愈合
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DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）