PHYTOMEDICINE
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2025
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IF 8.3
Lei Zhou,Leyuan Huang,Guanfeng He,Haixin Li,Manchun Liu,Jingwen Xu
Background Allergic rhinitis (AR) is a common IgE-mediated inflammatory disease of the nasal mucosa, involving immune–neural interactions such as mast cell activation, cytokine release, and transient receptor potential vanilloid 1 (TRPV1)-mediated neuronal sensitization. Xiao-Qing-Long-Tang (XQLT) is a classical traditional Chinese medicine used clinically for AR. However, its mechanisms, particularly in macrophage regulation and TRPV1 activity, remain not fully understood. Objective This study aimed to evaluate the therapeutic effects of XQLT in an ovalbumin (OVA)-induced AR mouse model and to investigate its molecular mechanisms focusing on immune regulation, macrophage-mediated inflammation, and TRPV1 channel activity. Methods The chemical composition of XQLT was analyzed by UPLC-Q Exactive Orbitrap-HRMS system. The therapeutic effectiveness of XQLT was assessed in an OVA-induced AR mouse model. Clinical symptoms, serum biomarkers (OVA-sIgE, interleukin-4 (IL-4), histamine), and histopathological changes were assessed. Transcriptomic analysis of nasal mucosa was performed to explore molecular pathways. The anti-inflammatory effects of XQLT were evaluated in LPS-stimulated RAW264.7 and bone marrow–derived macrophages by measuring NO, cytokine expression, and NF- κ B activation. TRPV1 involvement was examined using immunohistochemistry in AR mice model, calcium imaging in HEK293 cells overexpressing TRPV1, as well as molecular docking. Results XQLT treatment significantly reduced nasal rubbing and sneezing frequencies in AR mice, decreased serum OVA-sIgE, IL-4, and histamine levels, and ameliorated nasal and lung histopathological remodeling without observable toxicity. Transcriptomic profiling revealed that XQLT modulated DEGs associated with immune response, inflammatory signaling, olfactory transduction, and sensory perception of pain. In macrophages, XQLT suppressed LPS-induced NO production, downregulated IL-6, IL-1 β , CCL2, iNOS, and COX-2 expression, and inhibited NF- κ B nuclear translocation. Importantly, XQLT reduced TRPV1 expression in AR nasal mucosa and inhibited TRPV1-mediated calcium influx in HEK293 TRPV1-overexpressing cells. Zingiberis Rhizoma (Ganjiang) was identified as a key herb contributing to TRPV1 inhibition in XQLT, supported by molecular docking analysis. Conclusion XQLT alleviates AR symptoms and tissue remodeling through coordinated suppression of macrophage-mediated inflammation and TRPV1-dependent neurogenic pathways. These findings provide novel mechanistic insights into XQLT as a safe and promising multi-target therapy for AR.
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高影响因子
Scientific Reports
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2023
·Vol. 13
·期 1
·1-13
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IF 4.6
Xu Rui-Qi,Ma Ling,Chen Timson,Zhang Wei-Xiong,Chang Kuan,Wang Jing
Biosurfactants are attracting much interest due to their potential application as therapeutic agents in the medical and cosmetic field. Previous studies have demonstrated that biosurfactant such as sophorolipid (SL) exhibits immunomodulatory effects. In this article, we found the potential of sophorolipid for inhibiting histamine-induced itch and preliminarily explored its molecular basis. First, behavioral tests indicated that SL can remit the histamine-induced scratching behaviors of mice. Second, SL can suppress the the calcium influx induced by histamine, HTMT and VUF8430 in HaCaT cells. RT-PCR analysis showed that the histamine-induced upregulation of mRNA levels of phospholipase Cγ1, 1,4,5-trisphosphate receptor (IP3R), and protein kinase Cα can be inhibted by SL, suggesting that SL may impede the PLC/IP3R signaling pathway activated by histamine. In further tests, the capsaicin-induced calcium influx can also be inhibited by SL. The immunofluorescence and molecular docking analysis indicated that SL acts as an inhibitor of transient receptor potential vanilloid-1 (TRPV1) activation to decrease calcium influx against stimuli. In summary, these results revealed that SL may inhibit histamine-induced itch by decreasing PLC/IP3R signaling pathway activation and modulating TRPV1 activity. This paper indicates that SL can be a useful treatment for histamine-dependent itch.
研究领域:
药理学
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皮肤病学
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分子生物学
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治疗学
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JOURNAL OF ETHNOPHARMACOLOGY
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2022
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IF 5.195
Liping Zhou,Mengyang Hao,Xinsheng Fan,Zishan Lao,Mengwen Li,Erxin Shang
Ethnopharmacological relevance Houpo Mahuang Decoction (HPMHD is one of the classic traditional Chinese prescriptions that has been used in the treatment of asthma. The therapeutic effects and mechanism of HPMHD in aggravated asthma remain to be explored, especially from the perspective of metabolomics and Transient Receptor Potential Vanilloid-1 (TRPV1)/Ca 2+ /Tight junction (TJ) regulation. Aim of the study To investigate the therapeutic and metabolic regulatory effects and the underlying mechanism of HPMHD in asthmatic rats. Materials and methods The asthmatic rats were administered with the corresponding HPMHD (at dosages of 5.54, 11.07, 22.14 mg/kg). Then inflammatory cells in peripheral blood and bronchoalveolar lavage fluid (BALF) were counted, the levels of interleukin (IL)-4 and IL-13 in BALF were measured, and the changes in enhanced pause (Penh) and pathological damage of lung tissues were also detected to evaluate the protective effects of HPMHD. The serum metabolic profile of HPMHD in asthmatic rats was explored using Ultra-High-Performance Liquid Chromatography-mass spectrometer (UHPLC-MS), and the regulatory effects on TRPV1 and TJs of HPMHD in asthmatic rats were detected by Western blotting analysis. In vitro , 16HBE cells were stimulated with IL-4 plus SO 2 derivatives and then administered HPMHD. The intracellular Ca 2+ regulated by TRPV1, and the expression levels of TRPV1 and TJ proteins (TJs) were then detected by calcium imaging and Western blotting. The effects were verified by inhibition of TRPV1 and in short hairpin RNA (shRNA)-mediated TRPV1 silencing cells. Results HPMHD significantly attenuated the airway inflammation of asthmatic rats, and reduced the levels of inflammatory cells in peripheral blood and BALF as well as the levels of IL-4 plus IL-13 in BALF. In addition, the airway hyperresponsiveness and lung pathological damage were alleviated. Serum metabolomic analysis showed that 31 metabolites were differentially expressed among the normal saline-, model-, and HPMHD-treated rats. Pathway enrichment analysis showed that the metabolites were involved in 45 pathways, among which, TJs regulation-relevant pathway was associated with the Ca 2+ concentration change mediated by the TRP Vanilloid channel. In vivo and in vitro experiments indicated that HPMHD reduced the concentration of intracellular Ca 2+ via suppressing the expression and activation of TRPV1, increased the expression of ZO-1, Occludin , and Claudin-3, and protected the integrity of TJs. Conclusion The current study indicates that HPMHD alleviates rat asthma and participates in the regulation of serum metabolism. The anti-asthma effects of HPMHD might be related to the protection of TJs by inhibiting the intracellular Ca 2+ concentration via TRPV1.
研究领域:
药理学
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免疫学
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代谢组学
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肺科学
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中医
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Biomaterials Research
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2023
·Vol. 27
·期 1
·1-15
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IF 11.3
Shi Jiachen,Ma Qiuling,Su Wenting,Liu Congyan,Zhang Huangqin,Liu Yuping,Li Xiaoqi,Jiang Xi,Ge Chang,Kong Fei,Chen Yan,Qu Ding
Background Conventional dissolving microneedles (DMNs) face significant challenges in anti-melanoma therapy due to the lack of active thrust to achieve efficient transdermal drug delivery and intra-tumoral penetration.Methods In this study, the effervescent cannabidiol solid dispersion-doped dissolving microneedles (Ef/CBD-SD@DMNs) composed of the combined effervescent components (CaCO3 & NaHCO3) and CBD-based solid dispersion (CBD-SD) were facilely fabricated by the “one-step micro-molding” method for boosted transdermal and tumoral delivery of cannabidiol (CBD).Results Upon pressing into the skin, Ef/CBD-SD@DMNs rapidly produce CO2 bubbles through proton elimination, significantly enhancing the skin permeation and tumoral penetration of CBD. Once reaching the tumors, Ef/CBD-SD@DMNs can activate transient receptor potential vanilloid 1 (TRPV1) to increase Ca2+ influx and inhibit the downstream NFATc1-ATF3 signal to induce cell apoptosis. Additionally, Ef/CBD-SD@DMNs raise intra-tumoral pH environment to trigger the engineering of the tumor microenvironment (TME), including the M1 polarization of tumor-associated macrophages (TAMs) and increase of T cells infiltration. The introduction of Ca2+ can not only amplify the effervescent effect but also provide sufficient Ca2+ with CBD to potentiate the anti-melanoma efficacy. Such a “one stone, two birds” strategy combines the advantages of effervescent effects on transdermal delivery and TME regulation, creating favorable therapeutic conditions for CBD to obtain stronger inhibition of melanoma growth in vitro and in vivo.Conclusion sThis study holds promising potential in the transdermal delivery of CBD for melanoma therapy and offers a facile tool for transdermal therapies of skin tumors.
研究领域:
药学
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生物医学工程
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肿瘤学
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药物递送系统
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高影响因子
BIOLOGICAL RESEARCH
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2025
·Vol. 58
·期 1
·1-22
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IF 4.6
Chen Hanbin,Li Guanghong,Deng Lin,Li Shuli,Huang Songqiang,Lee Simon Ming-Yuen,Nie Xiaowei,Bian Jin-Song
Background Pain serves as a vital protective mechanism triggered by tissue damage. While NSAIDs and opioids offer relief, their prolonged usage is hindered by adverse effects. Developing analgesics with fewer side effects is crucial for effective pain treatment. The TRPV1 channel is a key target for pain relief, with its inhibitors effectively reducing hyperalgesia in animals. This research utilized virtual screening to identify TRPV1-selective natural compounds for potent analgesic properties. Results The physcion exhibited the notable affinity for TRPV1 compared to the compounds examined. After conducting molecular dynamics simulations, physcion emerged as the compound demonstrating the highest binding affinity towards TRPV1, a finding corroborated by calcium imaging, which validated its inhibitory impact. Furthermore, physcion mitigated the stretch number in the acetic acid-induced stretching model, prolonged the latency period in the hot water tail-flick and hot plate assays, and heightened the pain withdrawal threshold lowered by complete Freund’s adjuvant (CFA). Notably, physcion exerted a marked effect in ameliorating bone cancer-induced pain in the hot plate and von Frey tests. Additionally, physcion diminished the levels of inflammatory cytokines and the mRNA expression of both inflammatory and calcium-related genes in the CFA-induced murine model. Furthermore, physcion downregulated the expression of inflammatory genes induced by tumor necrosis factor-α (TNF-α) in RAW264.7 cells. The underlying mechanism potentially involves the suppression of the NF-κB and MAPK signaling cascades. Conclusions Our investigation underscores the potential of physcion as a promising candidate for analgesic therapy.
研究领域:
药理学
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疼痛研究
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分子生物学
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计算生物学
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炎症研究
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神经药理学
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肿瘤学
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药物研发
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ADVANCED FUNCTIONAL MATERIALS
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2023
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IF 19
Xinyue Shao,Chang Qu,Guoqiang Song,Binghao Wang,Qingyun Tao,Ran Jia,Junwei Li,Jinping Wang,Hailong An
Multidrug resistance (MDR) caused by overexpressed P-glycoprotein (P-gp) in cell membrane is the main barrier for clinical tumor chemotherapy. P-gp can pump the chemical drugs out of tumor cells depending on ATP-provided energy. Herein, a photothermal-driven intracellular magnesium ion (Mg 2+ ) regulation strategy is proposed to reverse drug resistance through constructing Mg 2+ - and doxorubicin (DOX, as model drug)-loaded bimetallic Pd@Pt nanostructure (DPd@PtM). Although DPd@PtM can deliver Mg 2+ into tumor cells through endocytosis, large amount of Mg 2+ releases outside cells. To this end, the photothermal effect of Pd@Pt nanostructure in the second near-infrared region is expected to activate the thermosensitive transient receptor potential cation channel subfamily V member 1 (TRPV1) channel for extracellular released Mg 2+ influx. Intercellular Mg 2+ accumulation suppresses tricarboxylic acid cycle to block intracellular adenosine triphosphate (ATP) production (cutoff energy supply for P-gp) and reduce O 2 consumption (downregulate P-gp expression), then inhibiting P-gp-mediated tumor MDR. Both in vitro and in vivo results demonstrate that DPd@PtM can open TRPV1 channel to elevate Mg 2+ level and then inhibit the P-gp activity to enhance intracellular DOX concentration for chemotherapy. It is believed that this photothermal-mediated tumor Mg 2+ regulation therapy based on reversing MDR is a promising strategy to kill cancer cells.
研究领域:
纳米技术
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癌症研究
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生物医学工程
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药物科学
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高影响因子
INFLAMMOPHARMACOLOGY
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2024
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IF 4.6
Li Ming-Jie,Xu Jing-Yi,Zhang Hua-Yue,Guo Min,Lan Meng-Ning,Kong Jie,Liu Shi-Wei,Zheng Hua-Jun
Alzheimer’s disease (AD) is a neurodegenerative disorder frequently accompanied by neuroinflammation and oxidative stress. The medicine and food homology (MFH) has shown potential for treating neuroinflammation and oxidative stress. This study aimed to provide a safe and efficient therapy for AD based on MFH. In this study, we develop a MFH formula consisting of egg yolk oil, perilla seed oil, raphani seed oil, cinnamon oil, and noni puree (EPRCN). To evaluate the ameliorative effects of EPRCN on AD-related symptoms, a mouse model of AD was constructed using intraperitoneal injection of scopolamine in ICR mice. Experimental results demonstrated that EPRCN supplement restored behavioral deficits and suppressed neuroinflammation and oxidative stress in the hippocampus of scopolamine-induced mice. An in vitro study was then performed using induction of Aβ (25–35) in glial (BV–2 and SW–1783) and neuron (SH–SY5Y) cell lines to examine the improvement mechanism of EPRCN on cognitive deficits. Multi-omics and in vitro studies demonstrated that these changes were driven by the anandamide (AEA)-Trpv1-Nrf2 pathway, which was inhibited by AM404 (an AEA inhibitor), AMG9810 (a Trpv1 inhibitor), and BT (an Nrf2 inhibitor). Consequently, EPRCN is an effective therapy on preventing cognitive deficits in mouse models of AD. In contrast to donepezil, EPRCN exhibits a novel modes action for ameliorating neuroinflammation. The mechanism of EPRCN on preventing cognitive deficits is mediated by improving neuroinflammation and oxidative stress via activating the AEA–Trpv1–Nrf2 pathway.
研究领域:
神经科学
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药理学
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分子生物学
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高影响因子
Korean Journal of Pain
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2024
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IF 3.4
Kaiwen Lin,Datian Fu,Zhongtao Wang,Xueer Zhang,Canyang Zhu
Background Galangin, commonly employed in traditional Chinese medicine for its diverse medicinal properties, exhibits potential in treating inflammatory pain. Nevertheless, its mechanism of action remains unclear. Methods Mice were randomly divided into 4 groups for 7 days a normal control group, a galangin-treated (25 and 50 mg/kg), and a positive control celecoxib (20 mg/kg). Analgesic and anti-inflammatory effects were evaluated using a hot plate test, acetic acid-induced writhing test, acetic acid-induced vascular permeability test, formalin-induced paw licking test, and carrageenan-induced paw swelling test. The interplay between galangin, transient receptor potential vanilloid 1 (TRPV1), NF-κB, COX-2, and TNF-α proteins was evaluated via molecular docking. COX-2, PGE2, IL-1β, IL-6, and TNF-α levels in serum were measured using ELISA after capsaicin administration (200 nmol/L). TRPV1 expression in the dorsal root ganglion was analyzed by Western blot. The quantities of substance P (SP) and calcitonin gene-related peptide (CGRP) were assessed using qPCR. Results Galangin reduced hot plate-induced licking latency, acetic acid-induced contortions, carrageenan-triggered foot inflammation, and capillary permeability in mice. It exhibited favorable affinity towards TRPV1, NF-κB, COX-2, and TNF-α, resulting in decreased levels of COX-2, PGE2, IL-1β, IL-6, and TNF-α in serum following capsaicin stimulation. Galangin effectively suppressed the upregulation of TRPV1 protein and associated receptor neuropeptides CGRP and SP mRNA, while concurrently inhibiting the expression of NF-κB, TNF-α, COX-2, and PGE2 mRNA. Conclusions Galangin exerts its anti-inflammatory pain effects by inhibiting TRPV1 activation and regulating COX-2, NF-κB/TNF-α expression, providing evidence for the use of galangin in the management of inflammatory pain.
研究领域:
药理学
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生物化学
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分子生物学
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炎症研究
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疼痛管理
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高影响因子
Redox Biology
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2026
·
IF 16.2
Yunshen Chen,Gaogao He,Wei Zhang,Jiajie Li,Xiaoxi Li,Sijun Dong,Qinglian Liu,Lei Zhou
By responding to stimuli of diverse physics and chemical nature, transient receptor potential (TRP) channels fulfill important physiological functions in both excitable and non-excitable cells. Capsaicin (CAP) from chili peppers and allyl isothiocyanate (AITC) from mustard are natural and potent agonists for TRPV1 and TRPA1, respectively. Upon exposure to hydrogen peroxide (H 2 O 2 ), the central molecule in redox signaling pathways, TRPA1 shows robust activation and much higher sensitivity than TRPV1. Singlet oxygen ( 1 O 2 ), the molecular oxygen in electrically excited states, is the least studied reactive oxygen species (ROS). Here we report that both TRPV1 and TRPA1 are sensitive to the modification by 1 O 2 , but they exhibit drastically different responses. 1 O 2 generated by excited photosensitizers enhances the function of TRPV1 by accelerating its opening kinetics, increasing the current amplitude, and left-shifting the voltage-dependent activation curve towards physiological membrane potentials. A histidine residue located in the N-terminal ankyrin repeat domain of TRPV1 is identified to be important in 1 O 2 modification process. In contrast, as reported by imaging of cytosolic calcium, 1 O 2 modification of TRPA1 leads to a transient increase and then permanent inhibition of channel activity, and eventually obliterates TRPA1's response to AITC but not carvacrol – electrophilic and non-electrophilic agonists for TRPA1, respectively. Conversely, hTRPA1 is much more sensitive to H 2 O 2 , with the EC50 for channel activation about five times lower than that of hTRPV1, and the responses by two channels to H 2 O 2 mainly involves intracellular cysteine residues. The physiological significance of the distinct responses of TRPV1 and TRPA1 to two representative ROS, 1 O 2 and H 2 O 2 , warrants further investigation.
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高影响因子
DIABETES OBESITY & METABOLISM
·
2026
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IF 6.1
Xingyu Yang,Linglong Zhang,Xiao Li,Yue Wu,Ziwei Yu,Xinyue Jing,Tiancheng Xu,Zhi Yu,Bin Xu,Li An,Mengjiang Lu
Aim Obesity impairs the colonic mucus layer and disrupts intestinal barrier function, leading to chronic inflammation. This study explores whether electroacupuncture can restore intestinal barrier integrity and alleviate chronic intestinal inflammation by promoting goblet cell mucus secretion via the TRPV1–CGRP–RAMP1 axis. It also examines the underlying mechanisms of sensory neuron. Epithelial cell crosstalk in this process, with the goal of providing a new interventional strategy for treating obesity-related intestinal barrier damage and metabolic inflammation. Materials and Methods In a high-fat diet (HFD)-induced obesity model using C57BL/6J mice, we employed tissue-clearing techniques to examine the expression of TRPV1 and CGRP in intact colon tissue. The expression of RAMP1 in goblet cells was assessed by immunohistochemistry. Colon pathology was evaluated using immunofluorescence, haematoxylin and eosin (H&E) staining, and Alcian blue-periodic acid-Schiff (AB-PAS) staining. Furthermore, western blot analysis was performed to measure the expression levels of tight junction proteins and proinflammatory cytokines in the colon tissue. Results HFD feeding resulted in increased intestinal permeability and aggravation of intestinal inflammation. Notably, electroacupuncture intervention reversed HFD-induced intestinal pathologies. Through targeted ablation of TRPV1 and administration of the RAMP1 antagonist BIBN4096, we further established the essential roles of TRPV1 signalling and the CGRP receptor RAMP1 in maintaining mucus layer thickness and intestinal homeostasis. Under these conditions, the therapeutic efficacy of electroacupuncture was abolished. Conclusions We demonstrated that electroacupuncture may promote mucus secretion from goblet cells via the TRPV1-CGRP-RAMP1 axis, thereby suppressing intestinal inflammation. This provides a feasible interventional strategy for treating obesity-related intestinal barrier damage.
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Advanced Science
·
2025
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IF 14.1
Xueying Cheng,Shuangyu Liu,Yu Zhang,Kang Peng,Muge Qile,Chao Wu,Mengyun Dou,Liu Liu,Na Yang,Rui Liu,Guiyang Zhang,Liangping Ni,Gaolin Liang,Fang Yang,Ye Zhang,Shufang He
The heat-sensitive transient receptor potential vanilloid 1 (TRPV1), which is highly expressed on cardiac sensory neurons, reportedly plays a crucial role in transmitting nociceptive signals from the heart to the spinal cord during myocardial ischemia and reperfusion. Here, iron oxide nanocubes (FeNCs) are developed that are conjugated with an antibody against the extracellular portion of TRPV1, and they are named FeNCs-TRPV1. In F11 cell line and primary dorsal root ganglion neurons, FeNCs-TRPV1 specifically activate TRPV1 channels and trigger Ca 2+ influx through magnetothermal effect under an alternating current magnetic field (ACMF). Intraspinally injected FeNCs-TRPV1 induced TRPV1 desensitization in rats exposed to repetitive and transient ACMF before ischemia, resulting in the inhibition of TRPV1-mediated Ca 2+ signaling and neuropeptide release in the spinal cord during myocardial ischemia and reperfusion. Consequently, FeNCs-TRPV1 reduce cardiac injury and ventricular arrhythmia, enhance the activity of prosurvival kinases, and inhibit myocardial cell apoptosis. These findings suggest that magnetic nanomaterials-mediated remote regulation of spinal TRPV1 can be a novel non-invasive neuromodulation therapy for the treatment of myocardial ischemia-reperfusion (IR) injury.
研究领域:
纳米医学
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心血管研究
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神经心脏病学
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生物医学工程
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分子神经科学
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高影响因子
Journal of Advanced Research
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2026
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IF 17.1
Yilu Sun,Weiyao Liao,Stephen Cho Wing SZE,Yibin Feng,Jianhui Rong,Jia Zhao
Introduction Microglia-mediated neuroinflammation hallmarks the pathophysiology of depression. We recently identified 6-shogaol (6Sh) from the ginger root ( Rhizoma Zingiberis Recens ) as a potent anti-neuroinflammatory and antidepressant drug candidate. Objectives This study aimed to resolve the bioavailability and cost-effectiveness of 6Sh for the development of novel anti-neuroinflammatory drugs against depression. Methods A biomimicry 6Sh analog (6SA) with an amide moeity is chemically synthesized by directly coupling vanillylamine with trans -2-octenoic acid and pharmacologically evaluated in a mouse model of corticosterone-induced depression. Single-cell RNA sequencing (scRNA-Seq) was performed to profile the brain spatial transcriptomic responses to 6SA for molecular insights to define the antidepressant mechanisms. Results As results, 6SA outperforms the parent 6Sh in terms of water solubility, oral bioavailability, cytotoxicity, cost-effectiveness and pharmacokinetic profile. Remarkably, 6SA more effectively attenuated neuroinflammation and depressive-like behaviors while demonstrated good safety profile in mice. Mechanistically, the scRNA-Seq results highlighted two important differentially expressed genes (i.e., Glul and lncRNA Gm57375) in the prefrontal cortex microglia. Strikingly, in vivo and in vitro experiments indicated that 6SA regulated Glul and Gm57375 expression in a TRPV1-dependent manner. Conclusion Thus, 6SA may be a promising drug candidate with the capacity to tune neuroinflammation via targeting the TRPV1–Glul–Gm57375 axis in microglia against depression.
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高影响因子
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