International Journal of Immunopathology and Pharmacology最新文献

{"title":"Dihydromyricetin improving myocardial function in the mice induced by CCl₄.","authors":"Wen-Juan Zhang, Ke-Yun Li, Le-Ying Lin, Tao Song, Heng Hu, Yi-Man Song, Zi-Qing Xiao, Jiang-Rui Zhu, Li-Tao Long, Gao-Lu Cao, Bin-Hong Huang","doi":"10.1177/03946320251317397","DOIUrl":"10.1177/03946320251317397","url":null,"abstract":"<p><strong>Objective: </strong>To study the role and underlying mechanisms of dihydromyricetin on the myocardial function in mice induced by CCl₄.</p><p><strong>Methods: </strong>Eighteen C57BL/6 mice (6-8 W, female) were randomly divided into the following three groups: control group, CCl₄-induced positive group (CCl₄ group), dihydromyricetin group, six mice/group. NLRP3-deficient (NLRP3^-/-) C57BL/6 mice used the same age, gender, and modeling method. The HL-1 cells were used for in vitro experiments. The HL-1 cells were treated with PBS, CCl₄, and CCl₄ + DMY respectively.</p><p><strong>Results: </strong>The RT-qPCR results showed that compared to the mice induced by CCl₄, the dihydromyricetin increased the Arg-1 mRNA level in the mouse myocardial tissues. The mRNA expressions of the iNOS, IL-33, and ST2 were reduced by the dihydromyricetin. The results of immunohistochemistry showed that dihydromyricetin decreased IL-33 protein expressions in the myocardial tissues. Western blot results also showed that compared with the control group, the activation of NLRP3 inflammasomes in the myocardial tissues of mice injured by CCl₄ was increased, and dihydromyricetin can reduce NLRP3 inflammasomes activation in the myocardial tissues induced by CCl₄. The results of ELISA showed that dihydromyricetin could reduce the IL-1β level in the serum of the mice induced by CCl_4. Consistent with the in vivo results, compared with the control group, the NLRP3 inflammasome activation and IL-33/ST2 expression were increased in the CCl₄-treated HL-1 cells, while DMY significantly weakened this effect. Interestingly, NLRP3 deficiency enhanced the protective effect of DMY on myocardial function in mice.</p><p><strong>Conclusions: </strong>IL-33/ST2 signaling pathways and NLRP3 inflammasome activation may be involved in dihydromyricetin improving the myocardial function of the mice induced by CCl₄.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251317397"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in mice.","authors":"Seona Park, Hyun Jung Lee, Seong-Joon Koh, Jong Pil Im, Joo Sung Kim","doi":"10.1177/03946320251398285","DOIUrl":"10.1177/03946320251398285","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to elucidate the anti-inflammatory mechanisms of asiatic acid (AA) by focusing on its modulation of the nuclear factor-κB (NF-κB) signaling pathway and to evaluate its therapeutic effects in murine models of both acute and chronic colitis.</p><p><strong>Introduction: </strong>AA, a naturally occurring triterpenoid compound derived from <i>Centella asiatica</i>, is known for its anti-inflammatory activity. However, its comprehensive effects on both acute and chronic intestinal inflammation, particularly through detailed modulation of the NF-κB pathway, have not been fully elucidated.</p><p><strong>Methods: </strong>Human intestinal epithelial cells COLO 205 and murine macrophage cells RAW 264.7 were pretreated with AA, followed by stimulation with tumor necrosis factor-α (TNF-α) or lipopolysaccharide (LPS), respectively. The mRNA expression of pro-inflammatory cytokines, including interleukin (IL)-8, TNF-α, and IL-6, was quantified using real-time RT-PCR. Western blotting was performed to assess the phosphorylation and degradation of the NF-κB inhibitor IκBα, and NF-κB DNA-binding activity was assessed via electrophoretic mobility shift assay (EMSA). In vivo, acute colitis was induced using dextran sulfate sodium (DSS) in wild-type mice, and chronic colitis was established by piroxicam administration in IL-10⁻/⁻ mice. Following AA treatment, colon length, body weight, histology (H&E) with histologic scoring, and colonic NF-κB p65 immunohistochemistry (IHC) were evaluated.</p><p><strong>Results: </strong>AA significantly downregulated cytokine expression in both cell lines. It inhibited IκBα phosphorylation and degradation, and EMSA demonstrated a marked reduction in NF-κB DNA-binding activity. In mice, AA attenuated body weight loss, colonic shortening, and histologic inflammation in both DSS and IL-10⁻/⁻ models. Concomitantly, colonic IHC showed reduced nuclear NF-κB p65.</p><p><strong>Conclusions: </strong>AA alleviates intestinal inflammation by suppressing NF-κB signaling in vitro and exhibits therapeutic efficacy in both acute and chronic colitis models, suggesting its potential as a therapeutic candidate for inflammatory bowel disease.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251398285"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12696327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145716509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Halofuginone induces ERK phosphorylation and synergizes with trametinib in gastric cancer cells.","authors":"Yuemin Sun, Peng Wang, Xiaofeng Bai, Liang Tian, Yuxin Zhong","doi":"10.1177/03946320251359860","DOIUrl":"10.1177/03946320251359860","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to investigate the effects of halofuginone (HF) on gastric cancer cells and whether the combination of HF and trametinib has synergistic effects.</p><p><strong>Introduction: </strong>Halofuginone, a natural small molecule isolated from the plant <i>Dichroa febrifuga</i>, has been found to have anticancer activity in a variety of cancers, but few studies on HF in gastric cancer.</p><p><strong>Methods: </strong>cell viability was performed using the CellTiterGlo assay and apoptosis and cell cycle analysis was performed by Annexin V-FITC staining and PI staining. We also analyzed RNA sequencing and differentially expressed genes was shown using the heatmap. Western blot and qPCR were carried out to determine the expression of pro-apoptotic and anti-apoptotic proteins.</p><p><strong>Results: </strong>HF inhibited proliferation and induced apoptosis in gastric cancer cells in a dose-dependent manner. HF induced the expression of p-ERK in gastric cancer cells. HF and trametinib synergistically inhibited the gastric cancer cell proliferation. Trametinib inhibited HF-induced p-ERK expression. HF reduced anti-apoptotic protein Mcl-1 expression and reduced trametinib-induced upregulation of Mcl-1 expression.</p><p><strong>Conclusion: </strong>HF exerts its anti-cancer effects in gastric cancer and has a synergistic inhibition with trametinib, which may provide a novel therapeutic strategy for gastric cancer.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251359860"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iron chelating, antioxidant and anti-apoptotic activities of hesperidin and/or rutin against induced-ferroptosis in heart tissue of rats.","authors":"Haidy A Abdullah, Fatma Sm Moawed, Esraa Sa Ahmed, Fatma F Abdel Hamid, Riham Abdel-Hamid Haroun","doi":"10.1177/03946320251331873","DOIUrl":"10.1177/03946320251331873","url":null,"abstract":"<p><p>Excess iron has been associated with cardiovascular diseases. Flavonoids are antioxidants and cardioprotectants. Therefore, the goal of the current study is to evaluate the anti-apoptotic, antioxidant, and iron-chelating qualities of two flavonoids, rutin (R) and hesperidin (H), as well as their potential to prevent induced ferroptosis in rats. It is an in vivo cross-sectional study, in which rats were divided into 12 groups; control, H, R, H + R, Fe, Fe + IR, Fe + IR + Ref, Fe + H, Fe + IR + H, Fe + R, Fe + IR + R and Fe + IR + H + R. Cardiac and serum iron levels, serum troponin I, creatine kinase-MB (CK-MB), total iron binding capacity (TIBC), transferrin, ferritin, and hepicidin were determined. Moreover, the levels of malondialdehyde (MDA), nitric oxide (NO) and glutathione (GSH) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), were also determined. The expression levels of DMT1, ACSL4, GPX4, Nrf2, and caspase-3 genes were evaluated by RT-qPCR. Lastly, a histological analysis of the heart tissues from several groups of rats was conducted. After hesperidin and/or rutin treatment, our results revealed that cardiac markers (serum troponin I and CK-MB), iron metabolism markers (serum and cardiac iron, TIBC, ferritin, transferrin, hepicidin and DMT1 expression levels) and oxidative stress markers (MDA, NO and ACSL4 expression levels) were significantly (<i>P</i> ⩽ 0.05) reduced, while the antioxidant markers (GSH level, GPx and SOD activities and GPX4 and Nrf2 expression levels) were significantly (<i>P</i> ⩽ 0.05) increased. Also, hesperidin and rutin exerted its protective anti-apoptotic role by significantly (<i>P</i> ⩽ 0.05) decreasing caspase-3 expression levels. Hesperidin and/or rutin treatment can be proposed as a therapeutic candidate to attenuate ferroptosis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"39 ","pages":"3946320251331873"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors and a model for prognosis prediction after intravenous thrombolysis with alteplase in acute ischemic stroke based on propensity score matching.","authors":"Pan Huang, XingYang Yi","doi":"10.1177/03946320241274231","DOIUrl":"10.1177/03946320241274231","url":null,"abstract":"<p><p><b>Background:</b> Alteplase intravenous thrombolysis is effective for treating acute ischemic stroke (AIS) within 4.5 h. Nevertheless, the prognosis remains poor for some patients.<b>Objective:</b> To investigate the risk factors for poor prognosis in patients undergoing intravenous thrombolysis with alteplase following AIS based on propensity score matching and to develop a predictive model.<b>Result:</b> Multivariate logistic regression analysis showed that baseline blood glucose (OR = 1.20, 95%CI, 1.03-1.39), baseline NIH Stroke Scale score (OR = 1.23, 95%CI, 1.12-1.35), and hyperlipidemia (OR = 6.60, 95%CI 1.74-25.00) were risk factors for poor prognosis in patients with AIS undergoing alteplase intravenous thrombolysis. Using these factors, a nomogram model was constructed for predicting patient prognosis at 3 months. The areas under the receiver operating characteristic curve (AUCs) of the training and validation groups were 0.792 (95CI% 0.715-0.870) and 0.885 (95CI% 0.798-0.972), respectively, showing good differentiation. The Hosmer Lemeshow goodness-of-fit test showed that the model had good fit. The calibration curve fitted well with the ideal curve, and the decision curve analysis curve showed that the model had good clinical applicability when the threshold probability was between 10%-80%.<b>Conclusion:</b> The established nomogram could successfully predict the 3-month prognosis of patients with AIS after undergoing alteplase intravenous thrombolysis. The model thus has clinical application value.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241274231"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11339746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improved gastric residence time of famotidine by raft-forming drug delivery system using DOE.","authors":"Rajalakshmi Munusamy, Sangeetha Shanmugasundharam","doi":"10.1177/03946320241249429","DOIUrl":"10.1177/03946320241249429","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the raft-forming suspension of famotidine as an anti-reflux formulation to improve the oral bioavailability of narrow absorption window drugs by enhancing gastric residence time (GRT) and preventing gastro-esophageal reflux disease (GERD).</p><p><strong>Method: </strong>Various combinations of raft-forming agents, such as Tragacanth gum (TG), guar gum (GG), and xanthan gum (XG), were evaluated alongside sodium alginate (SA) to develop an effective raft. Preformulation studies and preliminary screening were conducted to identify the most suitable raft-forming agent, and GG was chosen due to its mucilaginous properties. The formulation was optimized using a 32 full factorial design, with the quantities of GG and SA as independent factors and apparent viscosity and in-vitro drug release (%) as dependent factors. The in vivo floating behavior study was performed for optimized and stabilized formulation.</p><p><strong>Results: </strong>Among the tested batches, F6 was selected as the optimized formulation. It exhibited desirable characteristics such as adequate raft weight for extended floating in gastric fluid, improved apparent viscosity, and a significant percentage of drug release at 12 h. A mathematical model was applied to the in-vitro data to gain insights into the drug release mechanism of the formulation. The stability of the suspension was assessed under accelerated conditions, and it demonstrated satisfactory stability. The formulation remains floating in the Rabbit stomach for more than 12 h.</p><p><strong>Conclusion: </strong>It concludes that the developed formulation has enhanced bioavailability in the combination of GG and SA. The floating layer of the raft prevents acid reflux, and the famotidine is retained for an extended period of time in the gastric region, preventing excess acid secretion. The developed formulations are effective for stomach ulcers and GERD, with the effect of reducing acid secretion by H2 receptor antagonists.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241249429"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11084990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corilagin relieves atherosclerosis via the toll-like receptor 4 signaling pathway in vascular smooth muscle cells.","authors":"Yujie Wang, Yiqing Li, Yunfei Chen, Jinqian Mao, Jingyu Ji, Shaojun Zhang, Pan Liu, Khrystyna Pronyuk, David Fisher, Yiping Dang, Lei Zhao","doi":"10.1177/03946320241254083","DOIUrl":"10.1177/03946320241254083","url":null,"abstract":"<p><strong>Introduction: </strong>Corilagin possesses a diverse range of pharmacologic bioactivities. However, the specific protective effects and mechanisms of action of corilagin in the context of atherosclerosis remain unclear. In this study, we investigated the impact of corilagin on the toll-like receptor (TLR)4 signaling pathway in a mouse vascular smooth muscle cell line (MOVAS) stimulated by oxidized low-density lipoprotein (ox-LDL). Additionally, we examined the effects of corilagin in Sprague-Dawley rats experiencing atherosclerosis.</p><p><strong>Methods: </strong>The cytotoxicity of corilagin was assessed using the CCK8 assay. MOVAS cells, pre-incubated with ox-LDL, underwent treatment with varying concentrations of corilagin. TLR4 expression was modulated by either downregulation through small interfering (si)RNA or upregulation via lentivirus transfection. Molecular expression within the TLR4 signaling pathway was analyzed using real-time polymerase chain reaction (PCR) and Western blotting. The proliferation capacity of MOVAS cells was determined through cell counting. In a rat model, atherosclerosis was induced in femoral arteries using an improved guidewire injury method, and TLR4 expression in plaque areas was assessed using immunofluorescence. Pathological changes were examined through hematoxylin and eosin staining, as well as Oil-Red-O staining.</p><p><strong>Results: </strong>Corilagin demonstrated inhibitory effects on the TLR4 signaling pathway in MOVAS cells pre-stimulated with ox-LDL, consequently impeding the proliferative impact of ox-LDL. The modulation of TLR4 expression, either through downregulation or upregulation, similarly influenced the expression of downstream molecules. In an in vivo context, corilagin exhibited the ability to suppress TLR4 and MyD88 expression in the plaque lesion areas of rat femoral arteries, thereby alleviating the formation of atherosclerotic plaques.</p><p><strong>Conclusion: </strong>Corilagin can inhibit the TLR4 signaling pathway in VSMCs, possibly by downregulating TLR4 expression and, consequently, relieving atherosclerosis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241254083"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11179462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141318658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COVID-19: A threat to the respiratory system.","authors":"Ghulam Rasool, Waqas Ahmed Khan, Arif Muhammad Khan, Muhammad Riaz, Mazhar Abbas, Aziz Ur Rehman, Saba Irshad, Saeed Ahmad","doi":"10.1177/03946320241310307","DOIUrl":"10.1177/03946320241310307","url":null,"abstract":"<p><p>The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), causes acute coronavirus disease-19 (COVID-19) that has emerged on a pandemic level. Coronaviruses are well-known to have a negative impact on the lungs and cardiovascular system. SARS-CoV-2 induces a cytokine storm that primarily targets the lungs, causing widespread clinical disorders, including COVID-19. Although, SARS-CoV-2 positive individuals often show no or mild upper respiratory tract symptoms, severe cases can progress to acute respiratory distress syndrome (ARDS). Novel CoV-2 infection in 2019 resulted in viral pneumonia as well as other complications and extrapulmonary manifestation. ARDS is also linked to a higher risk of death. Now, it is essential to develop our perception of the long term sequelae coronavirus infection for the identification of COVID-19 survivors who are at higher risk of developing the chronic lung fibrosis. This review study was planned to provide an overview of the effects of SARS-CoV-2 infection on various parts of the respiratory system such as airways, pulmonary vascular, lung parenchymal and respiratory neuromuscular system as well as the potential mechanism of the ARDS related respiratory complications including the lung fibrosis in patients with severe COVID-19.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241310307"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11672396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress of research into microglial mediation of central post-stroke pain.","authors":"Yue-Rong Li, Zhao-Hui Dang, Shan-Shan Li, Guang-Ya Li, Hao-Bin Cai, Yun-Wei Lu, Lin-Lin Xie, Li-Ling Li, Liu-Ling Huang, Xiu-De Qin, Fan Bu","doi":"10.1177/03946320241309220","DOIUrl":"10.1177/03946320241309220","url":null,"abstract":"<p><p>Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that commonly occurs after cerebral stroke, and it severely impairs the daily activities of stroke patients. A number of fundamental and clinical studies support the theory that CPSP is mainly caused by ischemic and hemorrhagic injury of the spinal-thalamic-cortical neural pathway. However, the underlying reasons of CPSP genesis and development are far from clear. In recent years, the majority of research focused on microglia, the main resident immune cells of the central nervous system, which highlighted its critical role in the regulation of CPSP. The present article concentrated on exciting discoveries of microglia in mediating CPSP from the perspectives of their bioactive factors, cellular receptors, and signaling pathways, in order to offer a convenient and easy-to-digest overview. In addition, the potential and challenges of several agents in clinical translation of CPSP treatment was discussed based on recent preclinical studies.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241309220"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment of systemic sclerosis complicated with pyoderma gangrenosum with adalimumab: A case report of a rare disease.","authors":"Chengqiang Ren, Cheng Yu, Maoquan Zhang, Ding Li, Yueyue Zhao","doi":"10.1177/03946320241300137","DOIUrl":"10.1177/03946320241300137","url":null,"abstract":"<p><p>Pyoderma gangrenosum (PG) is a rare noninfectious neutrophilic dermatosis characterized by recurrent, painful ulcers that commonly affect the lower extremities but can also involve other parts of the body. Over half of patients with PG have concomitant systemic immune diseases, with the association of PG with systemic sclerosis (SSc) being extremely rare. Treatment of PG primarily involves local therapy, steroids, and immunosuppressants, with an increasing emphasis on biologic agents. Among these, tumor necrosis factor-alpha (TNF-α) antagonists are considered effective. The patient in this report was an elderly female with a history of systemic sclerosis for many years and initially presented with gangrenous ulcers on the fingertips. After inconclusive conventional treatment, adalimumab was added for 5 weeks, resulting in disease suppression, a reduction in ulcer size, and re-epithelialization of the skin lesions after 6 months.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241300137"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}