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ENERGY & FUELS · 2026 · IF 6

Environmental Self-Enhancement in PAM/SA Hydrogels: A Strategy for Deep Conformance Control in Heterogeneous Reservoirs

Shuai Zhou,Qiuyan Quan,Hongke Yang,Zhi Ye,Xueli Long,Tinglei Liu,Haien Yang,Dongzhi Yang

This study systematically investigates the swelling, time-dependent mechanical decay, and degradation of polyacrylamide (PAM)-based gels under simulated high-temperature reservoir conditions. A Ca2+-induced “environmentally self-enhancing” PAM/sodium alginate (SA) composite gel was designed to alleviate the pronounced performance decline caused by swelling and degradation. In this system, progressive cross-linking between SA and Ca2+ in formation water leads to the formation of an interpenetrating network (IPN), which contributes to improved structural stability. Experimental results indicate that incorporating 1.5% SA into a 20% PAM gel increases the swelling strength by a factor of 6.7, while the three-month strength retention improves from 14% to 50%. The composite gel also shows enhanced fatigue resistance and a delayed swelling response. In addition, PAM/SA microspheres prepared via inverse emulsion polymerization exhibit improved mechanical robustness after Ca2+ cross-linking, with the elastic modulus increasing by 36%. Core flooding experiments show that PAM/SA microspheres are able to gradually form stable plugging structures in porous media. After 7 days of swelling, the plugging ratio increases by 23% and the oil displacement efficiency improves by 3% compared with PAM microspheres. Microfluidic visualization further indicates that swollen microspheres form reconfigurable deposits within pore throats, which suppress preferential flow. Both the plugging pressure and the frequency of pressure fluctuations increase noticeably, and the displacement efficiency rises by 4%, reflecting enhanced flow field regulation. Overall, this study provides cross-scale experimental evidence for the environmentally induced strengthening mechanism of PAM/SA gels and suggests their potential application in deep conformance control.

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HUMAN REPRODUCTION · 2026 · IF 6.8

Decoding serotonin in endometriosis: unveiling its role in disease pathogenesis via the gut–reproductive microbiota axis

Wang Xinlei,Jia Yan,Wang Chao,Li Danyang,Guo Xiaoping,Jiang Shengyu,Zhou Zhengjie,Gao Chencheng,Wang Fang

STUDY QUESTIONHow can the potential mechanisms and targets of endometriosis be explored through multi-omics and multi-location approaches?SUMMARY ANSWERThis exploration of the gut–reproductive axis in patients with endometriosis found that serotonin is elevated in endometriosis and promotes disease progression through enhanced cell proliferation and inflammation.WHAT IS KNOWN ALREADYEndometriosis is a common inflammatory disease. Recent studies indicate that peripheral serotonin, which is regulated by the gut microbiota, can promote the progression of irritable bowel syndrome and various cancers.STUDY DESIGN, SIZE, DURATIONThis cross-sectional study enrolled 22 endometriosis patients and 22 control patients with uterine fibroids (surgical cases, October 2022–June 2023). Samples of vaginal secretions, endometrial tissue, peritoneal lavage fluid, feces, and ectopic lesions were collected from both groups. For validation, serum samples were added from 20 additional endometriosis patients and 20 healthy reproductive-age volunteers.PARTICIPANTS/MATERIALS, SETTING, METHODSThis study employed 16S rRNA gene sequencing to analyze the microbiota in the vagina, endometrial tissue, peritoneal fluid, and feces of patients with endometriosis and control groups, complemented by untargeted metabolomic analysis of peritoneal fluid. The results identified serotonin as a key metabolite and revealed specific bacterial species, shared between the reproductive and gastrointestinal tracts of endometriosis patients, which were significantly correlated with serotonin levels. Mendelian randomization analysis was conducted to explore the relationship between serotonin, these bacterial species, and endometriosis. Serum serotonin levels in endometriosis patients, BALB/C mouse models, and their respective controls were measured using ELISA. Immunohistochemistry and fluorescence staining were used to detect the expression of serotonin and its receptors in both ectopic and normal endometrium. The effects of serotonin on the biological behavior of various endometriosis cell models, including proliferation, migration, invasion, and apoptosis, were investigated using CCK8 assay, wound healing test, Transwell assay, apoptosis detection, ELISA, transcriptomics, and qPCR. The impact of serotonin on BALB/C mouse models was evaluated using H&E staining, flow cytometry, and ELISA.MAIN RESULTS AND THE ROLE OF CHANCEWe identified a significant enrichment of Akkermansia muciniphila (a bacterium shared by the gut and reproductive tract) in endometriosis patients, which positively correlated with peritoneal serotonin levels; Mendelian randomization analysis linked both to elevated endometriosis risk. Serotonin levels were elevated in patients’ serum (using mouse models) and in ectopic endometrium, in comparison to those of controls. In vitro, serotonin boosted endometriosis cell proliferation, migration, invasion, and inflammation, with upregulated IL-17/NF-κB pathways. In mice, serotonin treatment increased lesion growth, cell proliferation, and inflammation.LARGE SCALE DATAN/A.LIMITATIONS, REASONS FOR CAUTION(a) The relatively limited sample size, together with potential imbalance in endometriosis ASRM stage distribution and cesarean section rates, may restrict the generalizability of our findings. In addition, due to the requirement for peritoneal lavage fluid collection, the control group could not consist of entirely healthy women, which may have resulted in a more conservative estimation of group differences. Serum sex hormone levels were not assessed; however, strict inclusion criteria and uniform surgical timing were applied to minimize hormonal confounding. Future studies incorporating cycle-phase–standardized hormone measurements may provide additional insights. (b) Dietary information was not collected in this study, despite the known influence of diet on gut microbiota composition and serotonin metabolism. (c) The direct causal relationship between Akkermansia muciniphila and elevated serotonin levels remains to be established and warrants further validation using germ-free mouse models or fecal microbiota transplantation approaches. (d) The precise mechanisms by which the gut–reproductive tract microbiota axis regulates local and systemic serotonin synthesis remain unclear and require further investigation.WIDER IMPLICATIONS OF THE FINDINGSOur study is the first to utilize a multi-omics approach combined with a joint analysis of the female gut–reproductive tract axis across multiple loci, revealing and validating a significant increase in serotonin levels in patients with endometriosis. This change may be regulated by the gut–reproductive microbiota axis. These findings provide new insights into the pathogenesis of endometriosis and identify potential targets for prevention and treatment.STUDY FUNDING/COMPETING INTEREST(S)This study was funded by the Jilin Provincial Key Laboratory of Precision Infectious Diseases (Grant No. 20200601011JC), Key Laboratory of Health and Family Planning Commission of Jilin Province (Grant No. 3D5200117426). The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.TRIAL REGISTRATION NUMBERChiCTR2300077490.

CAS / MDL: 50-67-9
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MATERIALS CHARACTERIZATION · 2026 · IF 6.2

In-situ reduction enabled anti-oxidation sintering of copper paste in air for power module packaging

Shijun Huang,Mulan Li,Zifeng Ding,Jingwen Liu,Chaoyang Zhang,Tingting Dong,Yuanyuan Zhang,Cai-Fu Li

With the development of power electronic devices fabricated by wide-bandgap semiconductors, whose working temperature can reach over 250 °C, the corresponding die-attach material also should be able to withstand such a high temperature. Cu paste is an effective material to interconnect the chip with the substrate, but oxidation of Cu particles during storage and sintering now inhibits its application. In order to avoid oxidation, a Cu paste with self-reducibility and antioxidation ability was prepared. The Cu paste was mixed with two reductants and pre-oxidized Cu nanoparticles. The reductants can not only reduce the oxide layer but also provide a reducing atmosphere during sintering in air. Therefore, the in-situ reduced Cu nanoparticles can promote the necking growth without oxidation and lead to a higher strength. The maximum shear strength of 46.44 MPa was achieved by the joints that sintered at 300 °C for 30 min. In addition, the grain size, grain orientation and dislocation density of Cu joints sintered for various time were analyzed by Electron Backscattered Diffraction (EBSD) to illustrate the sintering mechanism. The initial grain boundary misorientation and the deformation strain from assisted pressure drive the grain boundary migration, leading to the formation of coherent interface, grain growth, dislocation accumulation and twin grain growth with the sintering time increased to 30 min. Therefore, the high shear strength was due to dislocation strengthening and twin grain strengthening.

CAS / MDL: 50-81-7
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ARCHIVES OF TOXICOLOGY · 2026 · IF 10.9

Mechanism-based inactivation of CYP2D6 by imperatorin and drug-drug interaction in vitro and in vivo

Wu Hualu,Cao Lu,Wang Peiqi,Li Ruibin,Wu Jun,Fu Haoxin,Chen Yan,Jiang Shiqi,Xu Ren-ai

Imperatorin (IMP) is a naturally occurring furanocoumarin with a wide range of pharmacological activities, including anti-cancer, anti-inflammatory, and anti-oxidant properties. This study preliminarily investigated the major cytochrome P450 (CYP) enzymes involved in the metabolism of IMP to heraclenin, identifying CYP3A4 as its primary metabolic enzyme. Furthermore, the impact of nine CYP3A4 variants on IMP metabolism was investigated, with CYP3A4.24 demonstrating the lowest relative clearance rate (6.26%). Additionally, the impact of napabucasin on IMP metabolism was investigated, revealing various degrees of inhibition in rat liver microsomes (RLM), human liver microsomes (HLM), and recombinant human CYP3A4. However, no significant alterations in pharmacokinetic parameters were observed during co-administration in rats. Mechanism-based inactivation studies revealed that IMP inactivated CYP2D6 in a time-, concentration-, and NADPH-dependent manner, with kinetic parameters of k inact = 0.024 min⁻¹ and K I = 2.814 µM. The competitive CYP2D6 inhibitor quinidine was found to attenuate this inactivation, while GSH or catalase/SOD did not demonstrate a similar effect. This observation suggested that the active intermediate acted within the enzyme’s active site. Subsequent to oxidation with potassium ferricyanide, there was partial recovery of CYP2D6 activity, thereby confirming the quasi-irreversible inactivator property of IMP. These findings suggested that IMP may exhibit clinically significant interactions with drugs metabolized by CYP2D6.

CAS / MDL: 2646-71-1
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ENVIRONMENTAL POLLUTION · 2026 · IF 7.2

Parental DEHP exposure induces sex-specific reproductive toxicity in zebrafish and behavioral deficits in unexposed offspring

Yanan Sun,Yuqing Fan,Yao Dang,Ping Ding,Xin Li,Gang Li,Haojie Luo,Jianliang Zhao,Guocheng Hu

Phthalates (PAEs) have attracted widespread attention as ubiquitous environmental contaminants. Among them, di-(2-ethylhexyl) phthalate (DEHP) is the most prevalent, particularly in the manufacturing of polyvinyl chloride. Although the direct toxic effects of DEHP on exposed individuals are well documented, far less is known about the potential for parentally transferred DEHP to induce adverse outcomes in unexposed offspring. In this study, adult zebrafish were chronically exposed to environmentally relevant concentrations of DEHP (0, 0.3, 3, and 30 μg/L) and subsequently spawned in DEHP-free water. DEHP accumulated in parental gonads and was transferred to unexposed F1 embryos. Compared to controls, offspring from parents exposed to 30 μg/L DEHP showed significantly increased embryo diameter and markedly impaired locomotor activity under light-dark cycles. Integrated multi-omics analysis further revealed that iba57 (mitochondrial function) and a2m3a (neurodevelopment) were consistently dysregulated at both mRNA and protein levels, linking the observed phenotypes to mitochondrial dysfunction and neurodevelopmental disruption. These findings demonstrate that even at environmentally relevant concentrations, parentally transferred DEHP can induce persistent effects in unexposed offspring, suggesting that current ecological risk assessment frameworks may underestimate the long-term risks of DEHP.

CAS / MDL: 67-68-5
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INTERNATIONAL JOURNAL OF PHARMACEUTICS · 2026 · IF 6

In situ injectable lyotropic liquid crystal depot for sustained taphalgin release in acute postsurgical pain management

Jian Zhang,Guangrui Liu,Keke Xie,Jie He,Anqi Zhu,Lanting Gao,Jing Li,Xiao Han,Yanna Lin,Chao Hao

Acute postsurgical pain (APSP) poses significant pain management challenges in clinical due to limitations of current analgesics in efficacy or safety. This study developed an in situ injectable lyotropic liquid crystal (LLC) depot for sustained release of Taphalgin (TAP), a tetrapeptide agonist of μ 1 -opioid receptors with potent analgesia and low side effects. A TAP-loaded hexagonal phase liquid crystalline (TAP/EG-LLC-Gel) was constructed by the self-assembly of glyceryl monooleate (GMO) and egg yolk phosphatidylcholine (EYPC) via solvent exchange of propylene glycol with aqueous solution, characterized through polarized light microscopy (PLM), small-angle X-ray scattering (SAXS), and rheological analysis. This TAP/EG-LLC-Gel demonstrated a cumulative release of 57.0 ± 2.6% (8 days) with mild initial burst release of 6.6 ± 1.8% (8 h), indicating favorable sustained release behaviors for TAP. Compared to free TAP, pharmacokinetic analysis revealed a 78-fold prolonged half-life (110.39 ± 30.10 h) for TAP/EG-LLC-Gel. The analgesic activity of TAP-LLC was evaluated in animal models of incision pain and acetic acid writhing, showing long-acting dose-dependent analgesia up to 8 days. This TAP-loaded in situ injectable LLC depot showed excellent sustained release behaviors with potent, long-acting and dose-dependent analgesia in two animal pain models, offering a promising solution for APSP management.

CAS / MDL: 93685-90-6
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MARINE POLLUTION BULLETIN · 2026 · IF 4.9

Roles of dissolved organic matter, Cl−, and NO3− in the photodegradation of β-estradiol in seawater

Diyi Liu,Lu Liu,Ping Yin,Yan Tian,Jing Zhang

17β-Estradiol (E2), a typical endocrine-disrupting chemical, is widely detected in various aquatic environments, including rivers, lakes, groundwater, estuaries, and coastal waters, posing significant ecological and health risks. Photodegradation is a key pathway for the transformation and removal of E2 from aquatic systems. This study investigated the effects of dissolved organic matter (DOM) from different sources and common inorganic anions (Cl − and NO 3 − ) on E2 photodegradation under simulated solar irradiation. The results indicated that the excited triplet state of DOM ( 3 DOM*), generated upon light absorption, was the key reactive species driving E2 photodegradation. Among the DOM sources examined, humic acid exhibited the strongest promotive effect on E2 photodegradation. Correlation analysis confirmed that terrestrial humic-like components within seawater DOM were the primary contributors to 3 DOM* formation. Seawater DOM from nearshore areas exhibited higher steady-state concentrations of 3 DOM* owing to greater terrestrial input. Both Cl − and NO 3 − effectively accelerated E2 photodegradation, and the E2 degradation rate increased with their concentrations. In contrast, the coexistence of Cl − , NO 3 − , and DOM inhibited E2 photodegradation. In DOM-dominated systems, the main transformation pathways of E2 involved oxidation and hydrolysis reactions on the phenolic ring. This study elucidates the effects of DOM source and water chemical composition on E2 photodegradation, which is crucial for accurately predicting its environmental fate and ecological risks. Moreover, the findings provide valuable insights into the photochemical transformation of other emerging organic contaminants.

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APPLIED CATALYSIS B-ENVIRONMENTAL · 2026 · IF 19.7

Sulfur-driven in situ oxygen vacancy engineering in TiO2 enables efficient photocatalytic transfer hydrogenation of furfural

Juwen Gu,Wanbing Gong,Yao Zhong,Yucui Liao,Minglei Sun,Jing He,Zhekang Peng,Xiaochun Li,Yuxiu Li,Bang Lan,Jun Ma,Tiejun Wang

Sulfur incorporation facilitates in situ oxygen-vacancy formation in TiO 2 . • S–O formation and S–V O coupling regulate the electronic structure of TiO 2 . • Oxygen vacancies promote furfural adsorption and activation. • Sulfur-mediated defect engineering enables selective furfural hydrogenation. • S 0.75 -TiO 2 achieves 44.0 mmol FA ·g cat. −1 ·h −1 with 99.5% FA selectivity. Photocatalytic transfer hydrogenation (PTH) of biomass-derived furfural (FF) to furfuryl alcohol (FA) using methanol as a green hydrogen donor represents a sustainable route for producing value-added chemicals, yet developing robust noble-metal-free catalysts remains challenging. Herein, we present a sulfur-doped TiO 2 photocatalyst exhibiting exceptional activity and selectivity for FF hydrogenation. The optimized catalyst delivers an impressive space-time FA yield of 44.0 mmol FA ·g cat. −1 ·h −1 with 99.5% selectivity under 500 mW·cm −2 irradiation, surpassing most state-of-the-art systems. Comprehensive characterizations and theoretical calculations reveal that lattice-substituted sulfur atoms form surface S–O species, driving oxygen vacancy formation and modulating the electronic structure of TiO 2 . The synergistic interaction between S species and V O sites regulates the electron density at active sites, thereby markedly promoting FF adsorption/activation, charge separation, and targeted hydrogenation. This work establishes a strategy for constructing high-efficiency, non-precious photocatalysts through sulfur-mediated oxygen-vacancy engineering. Download: Download high-res image (135KB) Download: Download full-size image

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ChemCatChem · 2026 ·Vol. 18 ·期 19 ·e00023 · IF 4.1

Current-Dependent Pathway Switching in Electrochemical Oxidative Dehydrogenation of Ethane Over an LSC Electrode in SOEC

Zhijie Wang,Jinxuan Hao,Hongpeng Fan,Xiao Lin,Linjuan Zhang,Jian-Qiang Wang

Electrochemical oxidative dehydrogenation (ODH) of ethane in solid oxide electrolysis cells (SOECs) offers a promising alternative to energy-intensive steam cracking. This work investigates the ODH mechanism using an LSC (La 0.6 Sr 0.4 CoO 3-δ ) anode in a 5 cm*5 cm single cell, achieving high ethylene selectivity (∼44%) at 650°C. In contrast, operation at elevated temperatures (e.g., 700°C) leads to anode degradation and a shift in selectivity. Through a combination of electrochemical impedance spectroscopy with distribution of relaxation times (EIS-DRT) and detailed product analysis, we reveal a decisive shift in the dominant reaction pathway governed by the applied current density. At low current densities, the direct electrochemical oxidation of ethane by surface oxygen species prevails. As the current increases, the mechanism transitions to a tandem process where the oxygen evolution reaction occurs first, followed by the thermochemical ODH of ethane. This mechanistic crossover is rationalized by the competition between ethane diffusion to active sites and the rate of electrochemical oxygen supply. These findings provide fundamental insights into the interplay of electrochemical and thermochemical steps in high-temperature alkane electrolysis, highlighting current density as a key lever for controlling selectivity. Graphical Current density acts as a key lever for steering ethane ODH pathways in SOECs. Over an LSC anode, low currents favor direct electrochemical oxidation by surface oxygen species. Higher currents shift the mechanism to a tandem process, where OER-generated O 2 drives thermochemical ODH. Moreover, thinner LSC anodes boost ethane diffusion into the active region, favoring direct oxidation and higher ethylene selectivity.

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ENVIRONMENTAL POLLUTION · 2026 · IF 7.2

Nanoplastics amplify ciprofloxacin-induced immunotoxicity: Oxidative stress in splenocytes and conformational and functional changes in lysozyme

Qianyue Yin,Yuntao Qi,Xiangxiang Li,Shuqi Guo,Shaoyang Hu,Xingchen Zhao,Wansong Zong,Jixin Su,Rutao Liu

NPs amplify CIP-induced immunotoxicity in splenocytes via oxidative stress. • Oxidative stress is a key driver of reduced splenocyte viability and inflammatory responses. • NPs@CIP disrupts LZM conformation and impairs its enzymatic activity. Nanoplastics (NPs) and ciprofloxacin (CIP), as emerging contaminants, widely coexist in the environment. Both NPs and CIP can accumulate in the spleen, suggesting a potential risk of immunotoxicity. However, studies on the mechanisms of immunotoxicity induced by combined exposure to NPs@CIP remain limited. The study found that NPs amplified the immunotoxic effects induced by CIP, manifested as splenocyte damage and conformational and functional changes in the immune factor lysozyme (LZM). At the cellular level, NPs exacerbated CIP-induced oxidative stress damage in splenocytes, as indicated by a burst in intracellular reactive oxygen species (ROS) levels (205.43% → 247.82%, +42.39%), increased consumption of superoxide dismutase (SOD) (52.20% → 48.77%, −3.44%), and greater accumulation of malondialdehyde (MDA) (179.95% → 190.25%, +10.30%), a final product of lipid peroxidation. This oxidative damage led to a further decrease in cell viability (54.05% → 48.09%, −5.96%), and exacerbated secretion of inflammatory cytokines TNF-α, IL-6, and IL-1β (+279.07, +25.28, +162.05 pg/mg prot), suggesting that oxidative stress not only induced splenocyte damage but triggered inflammatory responses. At the molecular level, we hypothesize that CIP adsorbed on the NP surface interacts with LZM, potentially forming an NPs-CIP-LZM ternary complex. This putative complex could exacerbate conformational and functional damage to LZM, manifesting as backbone denaturation, loosening of secondary structure, perturbation of the Trp microenvironment, and decreased enzymatic activity. This study provides mechanistic insights into the dual pathways through which NPs may amplify CIP-induced immunotoxicity, offering a theoretical basis for the mechanistic understanding of NPs toxicity and for risk evaluation strategies. Download: Download high-res image (354KB) Download: Download full-size image

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CHEMICAL ENGINEERING JOURNAL · 2026 · IF 12.5

Synergistic mechanisms of iron-carbon micro-electrolysis in promoting arsenic reduction and remediation in aquatic sediment

Wenjun Dong,Yan Kang,Zizhang Guo,Haoqin Ma,Boya Kuang

Combination of biochar and iron oxide enhanced As(III) oxidation in aquatic sediment. • Increased fulvic and humic acid DOM favored for iron cycle and bioavailable carbon source. • Iron and biochar amendment improved sucrase, urease and catalase activity. • Iron-biochar enriched enzymes abundance that related to As cycling, glycolysis and TCA. Arsenic (As) is ubiquitous in the aquatic environment, among which arsenite (As(III)) possessing extreme toxicity and environmental risk. Adding biochar is an extensive strategy for As remediation in sediment via immobilization, while the redox transformation of As is often ignored. Considering the effect of iron‑carbon micro-electrolysis on interspecies electron transfer, the present study intends to explore the role of biochar and iron oxide in the behavior of As in aquatic sediments, and elucidate the underlying mechanisms among iron‑carbon-As. Results reflected that the synergistic effect of biochar and magnetite reduced 40.7% of As(III) contents in sediment, related to the As(III) transformation rate of 27.4%, which were 14.6%, 26.6%, 29.7% higher than that in magnetite, biochar, and control groups, respectively. Correspondingly, the co-existence of biochar improved the generation of Fe(II) by 15.6%, indicating the increased inorganic electrons and iron dependent oxidation of As(III). It was attributed to the degradation of soluble organic carbon and increased proportions of fulvic acid-like and humic acid-like materials, which could also provide carbon source for microbial As metabolism. The iron and biochar up-regulated the abundance of catalase, and microbes that related to As metabolism like Bacteroidota , Acidobacteriota , and Chloroflexota , which reduced the bioavailability of As and alleviated their toxic pressure to sediment. They also increased the expression of arsR and arsC that related to As remediation, and enzymes in glycolysis (like K00134, K00927) and TCA (like K00024, K00031), which contributed to higher metabolic efficiency. This study provided comparative findings on the synergistic mechanisms of biochar and magnetite in enhancing As(III) oxidation, and provided an effective strategy for sediment remediation.

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INTERNATIONAL IMMUNOPHARMACOLOGY · 2026 · IF 5.6

Curcumin attenuates uterine pain in mice through suppression of neuroinflammation in the DRG and spinal cord

Ya-Ru Yang,Ji-Tao Tang,Bing-Qiang He,Lin-Xia Zhao,Huan-Jun Lu,Ling-Jie Ma,Yong-Jing Gao

Uterine pain associated with labor, dysmenorrhea, or endometriosis is often driven by inflammation, which enhances nociceptive signaling and contributes to hyperalgesia. Although nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids are commonly prescribed, their clinical application is limited by side effects, and a subset of patients exhibit inadequate or no response to NSAID therapy. Curcumin, a natural polyphenol extracted from Curcuma longa , exhibits well-documented anti-inflammatory and analgesic properties. In this study, we investigated the analgesic efficacy and underlying mechanisms of curcumin in a mouse model of uterine pain. Both intraperitoneal and intrathecal administration of curcumin significantly reduced writhing responses and improved locomotor performance in open-field tests. Molecular analyses revealed that estrogen and oxytocin treatment induced activation of glial cells in the dorsal root ganglia (DRG) and spinal cord. Intrathecal curcumin attenuated the activation of satellite glial cells and macrophages in the DRG, suppressed MAPK signaling (ERK, JNK, and p38), and decreased the expression of proinflammatory mediators, including IL-6, TNF-α, IL-1β, CCL2, and CXCL1. Similarly, in the spinal cord, curcumin reduced astrocyte and microglia activation, MAPK phosphorylation, and inflammatory cytokine and chemokine levels. Moreover, curcumin diminished p-ERK expression in DRG neurons and reduced c-Fos expression in the spinal dorsal horn. Collectively, these findings demonstrate that curcumin alleviates uterine pain by suppressing glial activation, MAPK signaling, and inflammatory mediators' production, ultimately reduces markers of neuronal activation and plasticity in the DRG and spinal cord. This provides mechanistic support for curcumin's potential in managing uterine pain.

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