Inflammopharmacology最新文献

{"title":"Effects of tranexamic acid on postoperative knee activity and stress, and inflammation cytokines in patients undergoing total knee arthroplasty.","authors":"Kenan Ma, Xiaobin Wu","doi":"10.1007/s10787-024-01619-4","DOIUrl":"https://doi.org/10.1007/s10787-024-01619-4","url":null,"abstract":"<p><strong>Background: </strong>Total knee arthroplasty (TKA) is an effective treatment for knee osteoarthritis, with postoperative bleeding and the inflammation-stress response being key factors that influence its outcomes. Tranexamic acid (TXA), an antifibrinolytic agent, has demonstrated efficacy in controlling perioperative bleeding. This study was to examine the effects of different doses of TXA on postoperative knee mobility and the inflammation-stress response in patients undergoing TKA METHODS: Ninety-eight patients undergoing unilateral TKA were randomly grouped based on the dose of TXA administered: 10 mg/kg (AG), 15 mg/kg (BG), and 20 mg/kg (CG). The bleeding, coagulation function, inflammation-stress cytokines, pain visual analogue scale (VAS) scores, knee mobility, and knee function hospital for special surgery (HSS) scores of the subjects were compared.</p><p><strong>Results: </strong>As the dose of TXA increased, the postoperative drainage volume, hidden bleeding, and total bleeding in TKA patients decreased, the levels of inflammatory factors interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) were reduced, the levels of stress factors malondialdehyde (MDA), angiotensin II (Ang II), and cortisol (Cor) were reduced, pain VAS scores decreased, and knee mobility increased, with an increase in functional HSS scores (P < 0.05).</p><p><strong>Conclusion: </strong>The administration of 20 mg/kg TXA in TKA patients visibly reduced bleeding following operation, improved the inflammation-stress response, and enhanced the function of the affected knee, which is beneficial to the postoperative recovery process.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmaceutical aspects of JAK inhibitors: a comparative review.","authors":"Sandhya Jinesh, Rajan Radhakrishnan","doi":"10.1007/s10787-024-01614-9","DOIUrl":"https://doi.org/10.1007/s10787-024-01614-9","url":null,"abstract":"<p><p>Janus kinase inhibitors (JAKIs) are a new class of drugs used in the treatment of a heterogeneous group of diseases, mainly inflammatory and autoimmune diseases. Janus kinase (JAK) is a family of non-receptor tyrosine kinases in cells that transduce cytokine-mediated signals. JAK, along with signal transducer and activator of transcription (STAT) protein, mediate important cellular processes such as immune response, carcinogenesis, cell differentiation, cell division, and cell death. Therefore, inhibitors of JAK-STAT signaling pathways could be useful in treating conditions mediated by the above-mentioned processes. JAK inhibitors mainly treat inflammatory and/or autoimmune diseases such as rheumatoid arthritis, psoriasis, and atopic dermatitis. In this review, we tried to focus on the discovery, pharmacology, and pharmaceutical aspects of JAK inhibitor drugs and their relative risks and benefits, especially focusing on the adverse effects of this class of drugs.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prooxidant state in anticancer drugs and prospect use of mitochondrial cofactors and anti-inflammatory agents in cancer prevention.","authors":"Giovanni Pagano, Alex Lyakhovich, Philippe J Thomas, Federico V Pallardó Catalayud, Luca Tiano, Adriana Zatterale, Marco Trifuoggi","doi":"10.1007/s10787-024-01613-w","DOIUrl":"https://doi.org/10.1007/s10787-024-01613-w","url":null,"abstract":"<p><p>An extensive body of literature has associated cancer with redox imbalance and inflammatory conditions. Thus, several studies and current clinical practice have relied on the use of anticancer drugs known to be associated with prooxidant state. On the other hand, a number of studies have reported on the effects of several antioxidants, anti-inflammatory agents and of mitochondrial cofactors (also termed mitochondrial nutrients, MNs) in counteracting or slowing carcinogenesis, or in controlling cancer growth. In the available literature, a body of evidence points on the roles of anti-inflammatory agents and of individual MNs against carcinogenesis or in controlling cancer cell proliferation, but only a few reports on the combined use of two or the effect of three MNs. These combinations are proposed as potentially successful tools to counteract carcinogenesis in prospective animal model studies or in adjuvant cancer treatment strategies. A \"triad\" of MNs are suggested to restore redox balance, mitigate side effects of prooxidative anticancer drugs, or aid in cancer prevention and/or adjuvant therapy. By elucidating their mechanistic underpinnings and appraising their clinical efficacy, we aim to contribute with a comprehensive understanding of these therapeutic modalities.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitexin mitigates oxidative stress, mitochondrial damage, pyroptosis and regulates small nucleolar RNA host gene 1/DNA methyltransferase 1/microRNA-495 axis in sepsis-associated acute lung injury.","authors":"Almaz Zaki, Mohd Mohsin, Salman Khan, Aman Khan, Shaniya Ahmad, Amit Verma, Shakir Ali, Tasneem Fatma, Mansoor Ali Syed","doi":"10.1007/s10787-024-01609-6","DOIUrl":"https://doi.org/10.1007/s10787-024-01609-6","url":null,"abstract":"<p><strong>Aim of the study: </strong>This study examined vitexin's effect on sepsis-induced acute lung injury. We used network pharmacology and in vivo and in vitro experiments were performed to elucidate vitexin's role in preventing pyroptosis and regulating small nucleolar RNA host gene 1 (SNHG1)/DNA methyltransferase 1 (DNMT1)/microRNA-495 (miR-495 axis.</p><p><strong>Materials and methods: </strong>We developed an acute lung injury model using C57BL/6 mice and MLE-12 cells. Through a combination of network pharmacology and in vitro screening, vitexin was identified as the most promising anti-inflammatory compound. Multiple techniques such as western blotting, real-time PCR, Hematoxylin and eosin staining, immunohistochemistry, and TUNEL assay were used. Additionally, immunofluorescence, DCFDA and TMRE staining, flow cytometry, methylation-specific PCR, and gene transfection techniques were performed to elucidate vitexin's potential targets and underlying mechanisms.</p><p><strong>Results: </strong>Vitexin treatment significantly reduced lung damage, neutrophil infiltration, and inflammation while improving tight junction integrity. In LPS-treated RAW264.7 macrophages and a septic mouse BALF-induced MLE-12 cell injury model, vitexin demonstrated anti-inflammatory effects, promoted M2 macrophage polarization, and enhanced regenerative markers. It also decreased oxidative stress, mitigated apoptosis and pyroptosis, and improved mitochondrial function. Our research uncovered a novel epigenetic regulatory mechanism involving lncRNA SNHG1, DNMT1, and miR-495.</p><p><strong>Conclusion: </strong>Vitexin's ability to reduce inflammation, counteract oxidative stress, and modulate epigenetic processes. These findings underscore the promising role of vitexin as a treatment for ALI generated by sepsis. The SNHG1/miR-495 axis, which has been identified, represents a new target for future therapies in acute lung injury.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyphenols mitigating inflammatory mechanisms in inflammatory bowel disease (IBD): focus on the NF-ƙB and JAK/STAT pathways.","authors":"Elysha Nur Ismail, Noraina Zakuan, Zulkefley Othman, Sharmili Vidyadaran, Hussin Mohammad, Reezal Ishak","doi":"10.1007/s10787-024-01607-8","DOIUrl":"https://doi.org/10.1007/s10787-024-01607-8","url":null,"abstract":"<p><p>The term \"inflammatory bowel disease\" (IBD) refers to a group of chronic inflammatory gastrointestinal disorders, which include ulcerative colitis and Crohn's disease. The necessity for alternative therapeutic approaches is underscored by the fact that although present medicines are successful, they frequently result in considerable adverse effects. Naturally occurring substances included in fruits and vegetables called polyphenols have been shown to have the capacity to control important inflammatory pathways including NF-κB and JAK/STAT, which are essential for the pathophysiology of IBD. The processes by which polyphenols, such as curcumin, EGCG, resveratrol, and quercetin, reduce inflammation are examined in this article. Polyphenols may have therapeutic advantages by blocking the synthesis of cytokines and the activation of immune cells by targeting these pathways. Preclinical study indicates a reduction in intestinal inflammation, which is encouraging. However, more clinical research is needed to determine the clinical relevance of polyphenols in the therapy of IBD, especially with regard to their long-term safety and bioavailability.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of quercetin in NLRP3-associated inflammation.","authors":"Jiaqi Wu, Tongtong Lv, Yu Liu, Yifan Liu, Yukun Han, Xin Liu, Xiaochun Peng, Fengru Tang, Jun Cai","doi":"10.1007/s10787-024-01566-0","DOIUrl":"10.1007/s10787-024-01566-0","url":null,"abstract":"<p><p>Quercetin is a natural flavonoid that is widely found in fruits and vegetables. As an important flavonoid, it exhibits a wide range of biological activities, including antioxidant, anti-inflammatory, antiviral, immunomodulatory, and analgesic activities. Quercetin exerts powerful antioxidant activity by regulating glutathione, enzyme activity, and the production of reactive oxygen species (ROS). Quercetin exerts powerful anti-inflammatory effects by acting on the Nod-like receptor protein 3 (NLRP3) inflammasome. In diabetes, quercetin has been shown to improve insulin sensitivity and reduce high blood sugar level, while, in neurological diseases, it potentially prevents neuronal degeneration and cognitive decline by regulating neuroinflammation. In addition, in liver diseases, quercetin may improve liver inflammation and fibrosis by regulating the NLRP3 activity. In addition, quercetin may improve inflammation in other diseases based on the NLRP3 inflammasome. With this background, in this review, we have discussed the progress in the study on the mechanism of quercetin toward improving inflammation via NLRP3 inflammasome in the past decade. In addition, from the perspective of quercetin glycoside derivatives, the anti-inflammatory mechanism of hyperoside, rutin, and isoquercetin based on NLRP3 inflammasome has been discussed. Moreover, we have discussed the pharmacokinetics of quercetin and its nanoformulation application, with the aim to provide new ideas for further research on the anti-inflammatory effect of quercetin and its glycoside derivatives based on NLRP3 inflammasome, as well as in drug development and application.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"3585-3610"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical efficacy of oral and nasal rivastigmine-loaded chitosan nano-particles on AlCl₃-induced Alzheimer's-like disease in rats.","authors":"Dina E ElMosbah, Marwa S Khattab, Marwa A Ibrahim, Mona I El-Asssal, Hala M F El Miniawy","doi":"10.1007/s10787-024-01541-9","DOIUrl":"10.1007/s10787-024-01541-9","url":null,"abstract":"<p><p>The successful treatment of Alzheimer's disease (AD) is still a big challenge. Rivastigmine is one of the most used drugs for the treatment of AD. The short half-life, lower bioavailability, and less concentration of the drug in the brain after oral delivery are considered the main drawbacks of rivastigmine. To improve these drawbacks, nanostructure-mediated drug delivery has gained more attention. This study investigates the effect of rivastigmine-loaded in optimized chitosan nano-particles (RS-CSNPs) as polymeric nano-carriers by different administration routes (oral and intranasal) on aluminum chloride (AlCl₃)-induced Alzheimer-like disease in rat. The model was established by giving rats 100 mg/kg/b.wt of AlCl₃ orally for 3 months. Then the experimental rats were treated with RS-CSNPs either orally or intranasally for 75 days. Histopathology, immunohistochemistry of Tau expression in brain tissue, and gene expression of Caspase-3, NF-κB, and Nrf-2 were carried out. The therapeutic agents used decreased the alterations observed in AlCl₃ group with improvement in the neuronal viability. In addition to low expression of tau protein, down-regulation of caspase-3 and NF-κB genes and up-regulation of Nrf-2. RS-CSNPs alleviated the progression of AD presumably via blocking the inflammatory cascade and decreasing the oxidative stress process. The intranasal route is superior to the oral one and promising in AD management.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"3943-3952"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141912503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leukotriene signaling in neurodegeneration: implications for treatment strategies.","authors":"Veerta Sharma, Prateek Sharma, Thakur Gurjeet Singh","doi":"10.1007/s10787-024-01557-1","DOIUrl":"10.1007/s10787-024-01557-1","url":null,"abstract":"<p><p>Leukotrienes (LTs) are a group of substances that cause inflammation. They are produced by the enzyme 5-lipoxygenase (5-LOX) from arachidonic acid. Cysteinyl LTs are a group of lipid molecules that have a prominent role in inflammatory signaling in the allergic diseases. Although they are traditionally known for their role in allergic disease, current advancements in bio-medical research have shed light on the involvement of these inflammatory mediators in diseases such as in the inflammation related to central nervous system (CNS) disorders. Among the CNS diseases, LTs, along with 5-LOX and their receptors, have been shown to be associated with multiple sclerosis (MS), Alzheimer's disease (AD), and Parkinson's disease (PD). Through a comprehensive review of current research and experimentation, this investigation provides an insight on the biosynthesis, receptors, and biological effects of LTs in the body. Furthermore, implications of leukotriene signaling in CNS and its intricate role in neurodegeneration are also studied. Through the revelation of these insights, our aim is to establish a foundation for the development of enhanced and focused therapeutic approaches in the continuous endeavor to combat neurodegeneration. Furthermore, the pharmacological inhibition of leukotriene signaling with selective inhibitors offers promising prospects for future interventions and treatments for neurodegenerative diseases.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"3571-3584"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atheroprotective role of vinpocetine: an old drug with new indication.","authors":"Mohammed H Abu-Alghayth, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Athanasios Alexiou, Marios Papadakis, Mostafa M Bahaa, Mohammed Afifi, Ammar Al-Farga, Eman Wahsh, Gaber El-Saber Batiha","doi":"10.1007/s10787-024-01529-5","DOIUrl":"10.1007/s10787-024-01529-5","url":null,"abstract":"<p><p>Endothelial dysfunction is considered one of the main causes of atherosclerosis and elevated blood pressure. Atherosclerosis (AS) formation is enhanced by different mechanisms including cytokine generation, vascular smooth muscle cell proliferation, and migration. One of the recent treatment toward endothelial dysfunction is vinpocetine (VPN). VPN is an ethyl apovincaminate used in the management of different cerebrovascular disorders and endothelial dysfunction through inhibition of atherosclerosis formation. VPN is a potent inhibitor of phosphodiesterase enzyme 1 (PDE1) as well it has anti-inflammatory and antioxidant effects through inhibition of the expression of nuclear factor kappa B (NF-κB). VPN has been shown to be effective against development and progression of AS. However, the underlying molecular mechanism was not fully clarified. Consequently, objective of the present narrative review was to clarify the mechanistic role of VPN in AS. Most of pro-inflammatory cytokines released from macrophages are inhibited by the action of VPN via NF-κB-dependent mechanism. VPN blocks monocyte adhesion and migration by inhibiting the expression of pro-inflammatory cytokines. As well, VPN is effective in reducing oxidative stress, a cornerstone in the pathogenesis of AS, through inhibition of NF-κB and PDE1. VPN promotes plaque stability and prevent erosion and rupture of atherosclerotic plaque. In conclusion, VPN through mitigation of inflammatory and oxidative stress with plaque stability effects could be effective agent in the management of endothelial dysfunction through inhibition of atherosclerosis mediators.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"3669-3678"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conventional DMARDs therapy decreases disease activity and inflammation in newly diagnosed patients with rheumatoid arthritis by increasing FoxP3, Sema-3A, and Nrp-1 gene expression.","authors":"Parviz Soufivand, Ghazal Hosseini Torshizi, Seyed Askar Roghani, Mohammad Dastbaz, Ramin Lotfi, Bijan Soleymani, Fatemeh Heydarpour, Zahra Abdan, Hosna Allahyari","doi":"10.1007/s10787-024-01565-1","DOIUrl":"10.1007/s10787-024-01565-1","url":null,"abstract":"<p><strong>Background: </strong>Semaphorins are axonal guidance molecules involved in neural development and contribute to the regulation of various phases of the immune response. This study aimed to investigate the plasma levels of the pro-inflammatory cytokine interleukin-6 (IL-6) and the regulatory T (Treg) cell-related cytokine interleukin-10 (IL-10), as well as the gene expression levels of forkhead box P3 (FoxP3), Semaphorin-3A (Sema-3A), Neuropilin-1 (Nrp-1), Semaphorin-4A (Sema-4A), and Plexin-D1 (Plxn-D1), in the peripheral blood of newly diagnosed rheumatoid arthritis (RA) patients treated with conventional disease-modifying antirheumatic drugs (DMARDs) for 6 months compared with healthy controls.</p><p><strong>Methods: </strong>Peripheral blood samples were obtained from 40 newly diagnosed RA patients (before and after treatment) and 40 age- and sex-matched healthy subjects. The plasma concentrations of IL-6 and IL-10 were quantified via enzyme-linked immunosorbent assay (ELISA), and the mRNA expression levels of FoxP3, Sema-3A, Nrp-1, Sema-4A, and Plxn-D1 were assessed via quantitative real-time PCR.</p><p><strong>Results: </strong>Compared with those in the controls, the plasma IL-6 levels in the RA patients (both pre- and post-treatment) were significantly greater (P < 0.001). Compared with the pre-treatment levels, the plasma IL-6 levels decreased significantly after DMARD therapy (P < 0.05). Moreover, plasma IL-10 levels were significantly greater in post-treatment RA patients than in controls (P < 0.05). The gene expression of FoxP3, Sema-3A, and Nrp-1 was significantly lower in pre-treated RA patients than in controls (P < 0.001). Compared with that in pre-treatment RA patients, the gene expression of FoxP3, Sema-3A, and Nrp-1 in DMARDs-treated RA patients was strongly increased (P < 0.05, P < 0.01, and P < 0.01, respectively). There was a positive correlation between Sema-3A gene expression and the gene expression of FoxP3 (r = 0.292, P < 0.01) and Nrp-1 (r = 0.569, P < 0.0001).</p><p><strong>Conclusion: </strong>Conventional DMARDs therapy effectively reduces disease activity and inflammation in newly diagnosed RA patients by increasing FoxP3, Sema-3A, and Nrp-1 gene expression.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"3687-3695"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}