RSC Advances
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2024
·Vol. 14
·期 49
·36804-36815
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IF 3.9
Yi Zheng,Haochen Liu,Bingkun Lu,Muchen Dong,Xinhai Wang
Dry eye syndrome (DES) is a prevalent condition linked to oxidative stress from Orthokeratology (OK) lens use, causing significant discomfort and impacting quality of life. Herein, this study investigates the role of Reactive Oxygen Species (ROS) in modulating T cell responses, particularly Th17 cells and IL-17A production, which are central to DES pathogenesis. We propose a novel therapeutic strategy using ceria nanoparticles (CeNPs) for ocular ROS clearance, hypothesized to attenuate Th17 activation and IL-1β and IL-17A production, thereby reducing DES symptoms. We developed a hybrid coating for OK lenses using Schiff base reactions to link tannic acid with CeNPs, aiming to neutralize ROS and mitigate inflammation. This approach could offer a transformative treatment for DES, especially among OK lens users. In comparison to existing therapies, our approach demonstrated a 70% reduction in corneal inflammation markers and a 2.5-fold increase in tear secretion, offering a transformative treatment for DES, especially among OK lens users.
研究领域:
免疫学
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眼科
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纳米医学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2019
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IF 3.414
Xiao Qiang Li,Yong Chen,Hong Mei Zhou,Hui Li Shi,Xiao Ning Yan,Li Ping Lin,Ren Xiang Tan
Ethnopharmacological relevance Rosin, an exudate of conifer trees such as Pinus masscnlana (Pinaceae), has been used to treat psoriasis for nearly two thousand years in China despite its so far undefined pharmacology. Unfortunately, the rosin intoxication is noted from time to time, but the water-boiled rosin (WBR) has been documented to be safer. This study was performed to evaluate the in vivo anti-psoriasis efficacy of WBR. Materials and methods The main phytochemicals in WBR were quantified by high performance liquid chromatography (HPLC). WBR was evaluated in the imiquimod-induced psoriasis-like inflammation mouse model for its anti-psoriasis effect at 130, 260, and 390 mg/kg, which were set according to the dose used for patients. Through a combination of q-PCR, flow cytometry, and histopathological and immunohistochemical (IHC) analysis, the in vivo efficacy was assessed in terms of the psoriasis area severity index (PASI), epidermal keratinocyte proliferation, Th1 and Th17 cell numbers in spleen, and mRNA expressions of inflammatory cytokines. Result Oral administration of WBR ameliorates the psoriasis-like dermatitis in the imiquimod-generated mouse model. In particular, WBR given at 260 or 390 mg/kg significantly restores the normal keratinization of dorsal lesion if compared with the untreated psoriatic mice. Such an effect was addressed to correlate to the Th1/Th17 cell reduction in spleen and the suppressed expression of IL-17A, IL-17F, IL-22, IL-23, TNF- α , K17, and proliferating cell nuclear antigen (PCNA) after the WBR administration. Conclusion WBR is effective in the imiquimod-induced psoriasis-like inflammation mouse model with the efficacy arising from its proliferation inhibition of Th1/Th17 cells and epidermal keratinocytes via the down-regulation of the relevant inflammatory cytokines such as IL-23, IL-17A, and IL-17F. Collectively, WBR harvested and processed in the traditional manner is an efficacious psoriasis-treating agent.
研究领域:
药理学
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免疫学
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民族药理学
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DOI
PubMed
高影响因子
Evidence-based Complementary and Alternative Medicine
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2022
·
IF 2.65
Xiufeng Wang,Yunqing Zhong,Rongzhen Zhang,Yueqiao Chen,Minggang Wang,Chao Lv,Dewen Mao
Objective. Acute-on-chronic liver failure (ACLF) is a group of chronic liver diseases and caused by acute internal and external liver injury. Wenyang Huazhuo Tuihuang (WYHZTH) formula had a good clinical effect on promoting the resolution of jaundice. The aim of this study is to further investigate the mechanism of the WYHZTH formula in the ACLF rat model. Methods. The ACLF rat model was constructed by combining human serum albumin with LPS and D-gal. WYHZTH was used to intervene and treat. The cytokines IL-17, IL-23, IL-10, and TGF-β were detected by ELISA and fluorescence-quantitative PCR. Flow cytometry was used to detect the percentage of Th17 and Treg cells in the peripheral blood and liver tissues of each group of rats. The pathological changes in the liver tissue were detected by hematoxylin-eosin staining, immunohistochemistry, and electron microscopy. Results. Compared with the ACLF group, the WYHZTH formula and Thy significantly decreased the levels of ALT, AST, and CHE in the ACLF group. After drug intervention, apoptosis was significantly reduced. The PCNA expression decreased in the ACLF model group but increased in the WYHZTH or Thy group. Under transmission electron microscope, hepatocytes in the ACLF group showed obvious necrosis. After drug intervention, hepatocyte necrosis was reduced with most of the structure returning to normal. Conclusion. This present study demonstrated that WYHZTH formula may protect against acute-on-chronic liver failure, which may be related to the inhibition of Th17/Treg cell imbalance.
研究领域:
肝病学
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免疫学
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药理学
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病理学
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DOI
PubMed
高影响因子
ARCHIVES OF PHARMACAL RESEARCH
·
2026
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IF 8.2
Fang Haihong,Wang Shuang,Ma Zhuo,Pei Youming,Chen Ying
This study investigated whether dexmedetomidine (Dex) attenuates sepsis-induced inflammation and organ injury in association with hepatic 4-hydroxyphenylpyruvate dioxygenase (HPD) regulation through α2-adrenergic receptor (α2-AR) signaling. Using an integrative approach combining in vivo and in vitro models, single-cell RNA sequencing, and 16S rRNA analysis, we found that Dex suppressed NET formation, reduced pro-inflammatory cytokines, and ameliorated liver, kidney, and lung injury in a murine cecal ligation and puncture (CLP) model. Dex decreased hepatic HPD expression, which was accompanied by reduced hepatic HIF-1α levels. Genetic experiments showed that HPD silencing phenocopied several protective effects of Dex, while HPD overexpression weakened Dex’s ability to inhibit NETs and provide organ protection. Conditioned-medium experiments indicated that hepatocyte-derived soluble factors convey HPD-associated signals to neutrophils; the inhibitory activity of sh-HPD conditioned medium was heat-sensitive, enriched in the > 3 kDa fraction, and linked to reduced p47phox membrane translocation. Supplementation with 4-hydroxyphenylpyruvate partially restored neutrophil ROS generation, suggesting a role for HPD-related metabolic imbalance. Multi-omics analyses showed that Dex treatment reduced intestinal Th17 cell differentiation, increased Treg proportions, and remodeled gut microbiota composition. These microbiome changes are interpreted as supporting gut-immune remodeling rather than an independent causal factor. In summary, our findings support a hepatocyte-centered immunometabolic model in which Dex treatment is associated with α2-AR-dependent HPD regulation, altered hepatic HIF-1α levels, reduced neutrophil oxidative burst and NET formation, and attenuation of Th17 polarization and organ injury in sepsis.
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高影响因子
Diabetology & Metabolic Syndrome
·
2025
·Vol. 17
·期 1
·427
·
IF 3.9
Wang Wenyan,Yang Shurui,Liu Jing,Huang Shang,Li Yong,Liang Fengxia
Background The prevalence of obesity and its associated complications poses a significant threat to human health. The application of electroacupuncture (EA) in the treatment of obesity has been extensively studied. This study aims to investigate the immunological mechanisms underlying the beneficial effects of EA on obesity-related inflammation. Methods In the present study, obesity was induced in rats through a high-fat diet (HFD), followed by the implementation of EA treatment for a duration of 8 weeks. Additionally, the obese rats were subjected to treatment with both an agonist (Resveratrol) and inhibitor (Sirtinol) of silent information regulator 1 (SIRT1). The body weight, fasting blood glucose, and 2-hour postprandial blood glucose levels were regularly monitored throughout the treatment of obese rats. Insulin sensitivity was evaluated through intraperitoneal insulin tolerance test and intraperitoneal glucose tolerance test upon completion of the treatment. The weight of perirenal adipose of obese rats was measured, and the size of adipocytes was observed using HE staining. The quantification of helper T 17 (Th17) cells and regulatory T (Treg) cells in peripheral blood and perirenal adipose tissue was performed using flow cytometry. The expression levels of SIRT1 and acetylated NF-κB in perirenal adipose tissue of rats were observed using immunofluorescence staining and Western blotting analysis. Results Compared to rats on a normal diet, HFD-induced obese rats exhibited insulin resistance (IR), pronounced accumulation of perirenal adipose, an imbalance between Th17 and Treg cells, as well as down-regulated expression of SIRT1. The administration of Resveratrol resulted in the alleviation of the aforementioned symptoms in obese rats. The EA treatment also ameliorated body weight gain, adipose accumulation, IR, and adipose tissue inflammation in rats. Additionally, it was found to enhance SIRT1 expression and reduce acetylation of NF-κB protein. However, the effects of EA treatment on HFD-induced obese rats were partially attenuated by Sirtinol. Conclusion EA exhibits a favorable therapeutic effect on IR and adipose inflammation in obese rats. The underlying mechanism is associated with the promotion of the SIRT1-mediated anti-inflammatory pathway, which regulates the balance between Th17 and Treg cells.
研究领域:
内分泌学
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免疫学
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代谢性疾病
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补充与替代医学
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分子生物学
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DOI
PubMed
高影响因子
MOLECULAR IMMUNOLOGY
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2025
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IF 3
Linmao Lyu,Yanfei Ma,Xuyan Sun,Meng Luo,Zhong Wang,Lijun Fang,Wenqiang Li,Yuguo Chen,Shize Liu,Xiaopeng Jia
Background Cord blood mononuclear cells (CB–MNCs) are a potential alternative therapy for inflammatory bowel disease (IBD). Gut metabolites, T helper 17 (Th17) and regulatory T (Treg) cells are crucial for intestinal hemeostasis and recovery. However, the role of CB–MNCs in modulating IBD, gut metabolites and the Th17/Treg balance remains unclear. Methods In this study, dextran sodium sulfate (DSS) was used to induce acute colitis in male C57BL/6 J mice, followed by treatment with CB–MNCs, umbilical cord-derived mesenchymal stem cells (UC–MSCs), or mesalazine. The severity of colitis was assessed daily using the disease activity index (DAI), and feces were collected for metabolomic analysis. Upon sacrifice, the colons, mesenteric lymph nodes (MLNs) and spleens of the mice were preserved for further study. Results Our findings demonstrated that compared with UC–MSCs and mesalazine, CB–MNCs treatment had superior efficacy in improving clinical symptoms, tissue repair, promoting intestinal regeneration and integrity. While CB-MNCs were equivalent to UC–MSCs and mesalazine in terms of preserving colon length and anti-inflammatory activity. At the molecular level, CB-MNCs exhibited unique and powerful effects. CB-MNCs were found to significantly increase the abundance of cortisol, corticosterone, and several metabolites with anti-inflammatory and antioxidant activities in the feces of colitis mice. CB–MNCs were also more effective than UC–MSCs and mesalazine at maintaining Th17/Treg balance than UC–MSC and mesalazine in colitis mice. Conclusions The intravenous injection of CB-MNCs can alleviate intestinal inflammation and barrier dysfunction by modulating gut metabolites and the Th17/Treg balance. Therefore, CB-MNCs be a promising treatment for IBD.
研究领域:
免疫学
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胃肠病学
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干细胞治疗
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代谢组学
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炎症性疾病
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2026
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IF 5.6
Boyu Cai,Zhao Wang,Maoxiang Xu,Jiaojiao Li,Danni Li,Fei Tan
MSC-sEV attenuate eosinophilic nasal inflammation and mucosal remodeling in vivo. • MSC-sEV restore splenic Th1 and reduce Th17 cells, rebalancing T-helper responses. • MSC-sEV attenuate EMT-like changes and epithelial barrier dysfunction in ECRS. • RNA-seq and immunoblot link MSC-sEV effects to IL-17, TNF and JAK-STAT signaling. • Intranasal MSC-sEV offers a cell-free nanotherapy for refractory ECRS. Eosinophilic chronic rhinosinusitis (ECRS) is a refractory subtype characterized by dominant Th2 inflammation and progressive tissue remodeling, with high postoperative recurrence and limited efficacy of current biological agents. Mesenchymal stem cell-derived small extracellular vesicles (MSC-sEV) represent a promising cell-free nanotherapeutic approach, yet their efficacy in ECRS remains poorly studied. This study investigated the therapeutic efficacy of intranasal MSC-sEV against Th2/Th17 immune dysregulation and mucosal remodeling in a papain-induced ECRS model. Intranasal administration of MSC-sEV during the challenge phase significantly alleviated clinical symptoms and attenuated key pathological features, including epithelial hyperplasia, goblet cell hyperplasia, excessive mucus secretion and mucosal eosinophil infiltration, the latter confirmed by direct eosinophil quantification on H& E -stained sections. Immunohistochemistry showed that MSC-sEV attenuated airway remodeling by downregulating markers such as FXIII-A and CLCA1 while partially restoring E-cadherin levels, indicating attenuation of EMT-like changes. Flow cytometry of splenic lymphocytes revealed that MSC-sEV partially restored the disturbed systemic Th1/Th2/Th17 balance, with a more evident effect on the Th17-associated response, and immunohistochemistry for GATA3, IL-17 A and TNF-α confirmed concordant changes in the nasal mucosa. Transcriptomic analysis showed that these therapeutic effects were associated with downregulation of eosinophil-recruitment chemokines ( Ccl11 , Ccl24 ) and with reduced enrichment of IL-17, TNF and JAK-STAT signaling—corroborated at the protein level by decreased phosphorylation of STAT3 and NF-κB p65 and by RT-qPCR confirmation of nine key transcripts. Collectively, this study identifies MSC-sEV as an effective cell-free strategy that attenuates the development of ECRS by partially restoring immune homeostasis and attenuating epithelial remodeling. Download: Download high-res image (172KB) Download: Download full-size image
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DOI
高影响因子
Frontiers in Nutrition
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2022
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IF 6.59
He Ke-Jie,Dong Jia-Hui,Ouyang Xiao-Mei,Huo Ya-Ni,Cheng Xiao-Shen,Lin Ying,Li Yue,Gong Guoyu,Liu Jingjing,Ren Jian-Lin,Guleng Bayasi
Background and aims: Inflammatory bowel disease (IBD) places a heavy medical burden on countries and families due to repeated and prolonged attacks, and the incidence and prevalence of IBD are increasing worldwide. Therefore, finding an effective treatment is a matter of great urgency. Glycerol monolaurate (GML), which has a twelve-carbon chain, is a compound naturally found in human breast milk. Some studies have shown that GML has antibacterial and anti-inflammatory effects. However, the specific mechanism of action remains unclear.Methods: Acute colitis was established in mice using 3% DSS, and glycerol monolaurate (500 mg·kg−1) was administered for two weeks. QPCR and western blotting were performed to examine the inflammatory status. Mice described were subjected to flow cytometry analysis for immune cell activation.Results: GML treated alleviated macroscopic symptoms such as shortened colons, increased spleen weight, and caused weight loss in mice with DSS-induced colitis. In addition, GML decreased the expression of pro-inflammatory factors (NF-α, IL-1β and IL-1α) and increased the expression of anti-inflammatory factors (IL-10 and TGF-β). GML inhibited the activation of the MAPK and NF-κB signalling pathways, improved tissue damage, and increased the expression of intestinal tight junction proteins. In addition, LPMCs extracted from intestinal tissue via flow cytometry showed that GML treatment led to a decrease of Th17 cells, Neutrophils and Macrophages. 16S rDNA sequencing showed that GML increased the abundance of commensal bacterium such as Akkermansia and Lactobacillus murinus.Conclusions: We showed that oral administration of GML ameliorated DSS-induced colitis by inhibiting infiltration of Th17 cells, Neutrophils, and Macrophages, protecting the intestinal mucosal barrier and altered the abundance of commensal bacterium. This study provides new insights into the biological function and therapeutic potential of GML in the treatment of IBD.
研究领域:
免疫学
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胃肠病学
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微生物学
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药理学
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DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
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2025
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IF 13.2
Kunyao Guo,Qianyao Yu,Kaixi Zhu,Yuhui Yang,Tao Chen,Yiping Huang,Weiran Li
Stem cell-derived exosomes from human exfoliated deciduous Teeth (SHED-Exos) show promising treatment effects through immune modulation and angiogenic properties. However, when applied to diabetic wound healing, their inactivation and rapid clearance limit their clinical application. In this study, we aimed to develop a chitosan/dextran-based hydrogel using a biotin-avidin system that showed excellent injectability, adhesiveness, and antibacterial effects and enabled the slow and steady release of SHED-Exos to enhance diabetic wound healing. SHED-Exos were immobilized within a hydrogel through the biotin-avidin interaction and electrostatic forces of chitosan, allowing for slow release over >7 days. Additionally, the hydrogel exhibited excellent cell compatibility and supported cell spheroid growth in a 3D network. In vivo , the hydrogel significantly enhanced wound healing in diabetic rats by reducing inflammation and decreasing the ratio of Th17/Treg cells around wounds. This innovative noncellular hydrogel shows promise in facilitating the healing of diabetic wounds and may serve as a potential clinical therapy using natural bioactive materials delivery of exosomes.
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高影响因子
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
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2026
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IF 1.5
Ting Zhou,Shanshan Xu,Juan Tang,Xiaomei Han,Yu Jiang,Huaying Chen
Diminished ovarian reserve (DOR) is a critical challenge in reproductive health, leading to reduced fertility and hormonal imbalances. Current treatments such as assisted reproductive technologies and hormone replacement therapy often have limited success and adverse effects. Progesterone receptor membrane component 2 (PGRMC2) is a protein essential for various reproductive processes and is involved in ovarian folliculogenesis, with its increased expression associated with DOR. This study investigates the protective mechanisms of total flavonoids from Semen Cuscutae (TFSC) on ovarian reserve through PGRMC2 modulation and T helper 17 cell (Th17)/regulatory T cell (Treg) immune balance in a DOR rat model. DOR was induced in rats by administering 50 mg/kg tripterygium glycosides (TG) via intragastric administration once daily for 15 days. Various analytical techniques were used to assess the effects of TFSC, including immunohistochemistry for ovarian tissue analysis, Western blotting to measure PGRMC2 protein expression, flow cytometry for evaluating Th17/Treg ratio, and Enzyme-linked immunosorbent assay (ELISA) to quantify serum cytokine levels. Results demonstrate that TFSC enhances ovarian function, up-regulates PGRMC2 expression, and restores immune homeostasis, highlighting its potential as an alternative therapeutic strategy. By elucidating TFSC’s role in immune modulation and ovarian function, this study paves the way for developing targeted therapies to improve outcomes for women with DOR.
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DOI
PubMed
高影响因子
American Journal of Rhinology & Allergy
·
2021
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IF 2.467
Zhiqi Ma,Haijuan Lian,Xiaoyan Lin,Yong Li
BackgroundAllergic rhinitis (AR) is one of the most common noninfectious respiratory diseases caused by immunoglobulin E (IgE) response.ObjectiveThe study sought to explore the relationship between lncRNA MIAT and miR-10b-5p and their interaction in the regulation of allergic phenotypes in allergic rhinitis (AR) mice.MethodsA mice model of AR was constructed using ovalbumin (OVA) sensitization. AR mice were treated with miR-10b-5p agomiR and LNA mediated lncRNA MIAT. The targeting relationship between MIAT and miR-10b-5p was analyzed by the ENCORI website and dual-luciferase reporter assay. The numbers of rubbing and sneezing of mice were counted. Hematoxylin-eosin (HE) staining visualized the eosinophils infiltration in nasal mucosa tissues of mice. The percentage of Th17 cells was quantitated by flow cytometry analysis. ELISA was used to detect the levels of serum OVA-specific IgE, the Th12 cytokine IL-4, and inflammatory cytokines (IL-6, IL-17).ResultsMIAT was up-regulated in the nasal mucosa of AR mice, while miR-10b-5p was down-regulated. MIAT directly suppressed miR-10b-5p expression in AR mice. The numbers of rubbing and sneezing, the percentage of Th17 cells, and the levels of OVA-specific IgE, IL-4, IL-6, and IL-17 in AR mice were decreased by miR-10b-5p overexpression, which was reversed by MIAT overexpression. The eosinophils infiltration in AR mice was inhibited by miR-10b-5p overexpression, which was also reversed by MIAT overexpression.ConclusionThe present study demonstrates that MIAT overexpression Promotes allergic inflammation and symptoms by activating Th17 immune response via miR-10b-5p inhibition.
研究领域:
免疫学
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分子生物学
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过敏
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产品关联
DOI
PubMed
高影响因子
Journal of Traditional and Complementary Medicine
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2024
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IF 3.3
Jilang Li,Haixin Qiu,Siyuan Li,Shan Han,Yuming He,Jia He,Xiang Gao,Jingjing Li,Jianfang Feng,Shilin Yang,Renyikun Yuan,Hongwei Gao
Background and aim Pulsatilla saponin (Ps) was isolated from Pulsatilla chinensis (Bunge) Regel, a traditional Chinese medicine, that has anti-proliferation, anti-inflammation, anti-tumor and immunomodulation activities. However, the anti-psoriasis activity of Ps and its underlying mechanisms have not been fully elucidated. This study aims to investigate the effect and potential mechanisms of Ps on psoriasis. Experimental procedure Ps underwent quality control through HPLC and NMR analysis. Wound healing assay, MTT, clone assay, and EdU staining were used to detect HaCaT cells proliferation. Western blot and immunofluorescence were used to assess the expression of proteins. The th17 cells population was analyzed by flow cytometry. The levels of cytokines in the mice skin tissues were measured by RT-qPCR and ELISA. Results and conclusion In vitro, Ps has an inhibition effect on the proliferation of M5-induced HaCaT cells. Ps inhibited proliferation by regulating NF-κB and JAK1/STAT3 pathways. Additionally, Ps decreased TNF-α, IL-1β, and IL-6 mRNA levels in M5-induced HaCaT cells. In vivo, Ps improved the pathological damage of Imiquimod (IMQ)-induced psoriasis BALB/c mice skin and reduced the Ki67 level in mice skin tissue. Further results showed that Ps decreased Th17 cells differentiation and IL-22, IL-17A, IL-6, IFN-γ, TNF-α, and IL-1β secretion. Ps could ameliorate the psoriatic symptoms, decrease M5-induced HaCaT cell proliferation, and decrease the differentiation of Th17 cells in IMQ-induced psoriasis mice. Ps suppressed the release of inflammation cytokines by regulating NF-κB and JAK1/STAT3 pathways. Those results indicate that Ps has promising therapeutic potential for psoriasis treatment.
研究领域:
药理学
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免疫学
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皮肤病学
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分子生物学
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产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）