Immunopharmacology and Immunotoxicology最新文献

{"title":"Ivermectin ameliorates bleomycin-induced lung fibrosis in male rats by inhibiting the inflammation and oxidative stress.","authors":"Fatemeh Habibi Razi, Razieh Mohammad Jafari, Mohammad Amin Manavi, Mohammad Sheibani, Amir Rashidian, Seyed Mohammad Tavangar, Mohammad Taghi Beighmohammadi, Ahmad Reza Dehpour","doi":"10.1080/08923973.2023.2298895","DOIUrl":"10.1080/08923973.2023.2298895","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF) is a pulmonary fibrotic disease characterized by a poor prognosis, which its pathogenesis involves the accumulation of abnormal fibrous tissue, inflammation, and oxidative stress. Ivermectin, a positive allosteric modulator of GABA_A receptor, exerts anti-inflammatory and antioxidant properties in preclinical studies. The present study investigates the potential protective effects of ivermectin treatment in rats against bleomycin-induced IPF.</p><p><strong>Materials and methods: </strong>The present study involved 42 male Wistar rats, which were divided into five groups: control (without induction of IPF), bleomycin (IPF-induced by bleomycin 2.5 mg/kg, by intratracheal administration), and three fibrosis groups receiving ivermectin (0.5, 1, and 3 mg/kg). lung tissues were harvested for measurement of oxidative stress [<i>via</i> myeloperoxidase (MPO), superoxide dismutase (SOD), glutathione (GSH)] and inflammatory markers (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β], and transforming growth factor-β [TGF-β]). Histological assessments of tissue damage were performed using hematoxylin-eosin (H&E) and Masson's trichrome staining methods.</p><p><strong>Results: </strong>The induction of fibrosis <i>via</i> bleomycin was found to increase levels of MPO as well as TNF-α, IL-1β, and TGF-β while decrease SOD activity and GSH level. Treatment with ivermectin at a dosage of 3 mg/kg was able to reverse the effects of bleomycin-induced fibrosis on these markers. In addition, results from H&E and Masson's trichrome staining showed that ivermectin treatment at this same dose reduced tissue damage and pulmonary fibrosis.</p><p><strong>Conclusion: </strong>The data obtained from this study indicate that ivermectin may have therapeutic benefits for IPF, likely due to its ability to reduce inflammation and mitigate oxidative stress-induced toxicity.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatoprotective actions of melatonin by mainly modulating oxidative status and apoptosis rate in lipopolysaccharide-induced liver damage.","authors":"Mukaddes Esrefoğlu, Tugce Kubra Kalkan, Ersin Karatas, Birsen Elibol, Emine Rumeysa Hekimoglu, Fatma Bedia Karakaya Cimen, Arzu Hanim Yay","doi":"10.1080/08923973.2023.2291751","DOIUrl":"10.1080/08923973.2023.2291751","url":null,"abstract":"<p><strong>Aim: </strong>One of the serious complications of sepsis is liver damage and liver failure. This study aimed to evaluate the protective and therapeutic potential of melatonin in rats with lipopolysaccharide-induced sepsis.</p><p><strong>Main methods: </strong>Female Spraque-Dawley rats received single a dose of 7.5 mg/kg lipopolysaccharide in saline to create a 24-h sepsis model. One of the other groups received melatonin at a dose of 10 mg/kg/day beginning 1 week before sepsis induction to the end of the experiment. The melatonin group received the same doses of melatonin for the same duration but not lipopolysaccharide. The vehicle group received the same doses of saline, the vehicle of melatonin, for the same duration. Twenty-four hours after the last injection, the rats were decapitated. By appropriate histochemical, immunohistochemical, biochemical, and molecular techniques, anti-necrotic, anti-apoptotic, anti-necroptotic, anti-inflammatory, and antioxidant effects of melatonin were assessed.</p><p><strong>Key findings: </strong>Lipopolysaccharide has disrupted liver functions by inducing oxidative stress, inflammation, necrotic, apoptotic, and necroptotic cell death, thus disrupting liver functions. Melatonin was found to be beneficial in terms of inhibiting the intrinsic pathway of apoptosis and tissue oxidant levels, stimulating tissue antioxidant enzyme levels, and restoring hepatocyte functions.</p><p><strong>Significance: </strong>Melatonin, at those doses and duration, was found to be hepatoprotective by mainly modulating oxidative status and apoptosis rate, however, failed to significantly reduce histopathological damage. We suggest that longer-term melatonin administration may produce anti-inflammatory and anti-necrotic effects as well.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138487374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of Vortioxetine on the NLRP3 pathway and microglial activity in the prefrontal cortex in an experimental model of depression.","authors":"Gulin Ozdamar Unal, Duygu Kumbul, Kuyas Hekimler Ozturk, Gamze Erkılınc, Feyza Donmez, Eltaf Dogan Kıran, Ramazan Oğuz Yuceer","doi":"10.1080/08923973.2024.2308268","DOIUrl":"10.1080/08923973.2024.2308268","url":null,"abstract":"<p><strong>Background: </strong>Increasing evidence suggests that early life stress (ELS) and neuroinflammation are associated with the pathophysiology of depression. The purpose of this study was to determine the effects of Vortioxetine (VOR), a novel antidepressant, on ELS-induced behavioral changes and neuroinflammation.</p><p><strong>Method: </strong>Wistar Albino 4-week-old male rats were divided into four groups: control; chronic unpredictable stress (CUMS), VOR, CUMS + VOR. Neurobehavioral assessment was performed on the first, 21st, and 42nd days. RT-PCR was used to detect the expression of P2X7, NLRP3, IL1β, IL18 in the prefrontal cortex. To assess the microglial activities of the prefrontal cortex, immunohistochemically stained CD68, and leukocyte common antigen (LCA) preparations were scanned with Manual WSI software, Basler camera, and scored.</p><p><strong>Result and discussion: </strong>Exposure to CUMS was associated with depression and anxiety-like behaviors, and administration of VOR led to improvement in these behaviors. NLRP3, IL-1β, and IL-18 were shown to be upregulated in the prefrontal cortex of CUMS rats, while their high expression was inhibited by VOR treatment. CD68 and LCA expressions were significantly higher in the CUMS group compared to the other groups.</p><p><strong>Conclusion: </strong>According to these results, it may be considered that NLRP3 inflammasome-associated neuroinflammatory response and microglial activation may play a role in the etiopathogenesis of ELS.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139570503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/08923973.2024.2314849","DOIUrl":"10.1080/08923973.2024.2314849","url":null,"abstract":"","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139697306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Songorine inhibits oxidative stress-related inflammation through PI3K/AKT/NRF2 signaling pathway to alleviate lipopolysaccharide-induced septic acute lung injury.","authors":"Jingjing Fang, Qin Huang, Chaolu Shi, Lei Gai, Xinnian Wang, Biqing Yan","doi":"10.1080/08923973.2023.2281902","DOIUrl":"10.1080/08923973.2023.2281902","url":null,"abstract":"<p><strong>Objective: </strong>The present study aimed to investigate the protective action and mechanism of songorine on sepsis-induced acute lung injury (ALI).</p><p><strong>Methods: </strong>The sepsis-induced ALI mouse and cell models were established by lipopolysaccharide (LPS) induction. Lung injury was assayed by hematoxylin and eosin staining, lung injury score, and lung wet-to-dry (W/D) weight ratio. Apoptosis in lung tissues was evaluated by TUNEL assay, and the expression of apoptosis-related markers (Bcl2, Bax, and caspase-3) was measured by western blotting. Levels of pro-inflammatory factors and oxidative stress markers in the bronchoalveolar lavage fluid (BALF) of mice were measured by ELISA and RT-qPCR. The expression of PI3K/AKT/NRF2 pathway-related proteins was analyzed by western blotting.</p><p><strong>Results: </strong>Songorine treatment at 40 mg/kg mitigated sepsis-induced ALI, characterized by improved histopathology, lung injury score, and lung W/D weight ratio (<i>p</i> < 0.05). Moreover, songorine markedly attenuated sepsis-induced apoptosis in lung tissues; this was evidenced by an increase in Bcl2 levels and a decrease in Bax and caspase-3 levels (<i>p</i> < 0.01). Also, songorine reduced levels of proinflammatory cytokines (TNF-α, IL-6, IL-1β and MPO) and oxidative stress regulators (SOD and GSH) in the BALF of LPS-induced sepsis mice and RAW264.7 cells (<i>p</i> < 0.05). In addition, songorine upregulated the PI3K/AKT/NRF2 pathway-related proteins in LPS-induced sepsis mice and RAW264.7 cells (<i>p</i> < 0.05). Furthermore, LY294002 (a PI3K inhibitor) treatment reversed the protective effect of songorine on sepsis-induced ALI.</p><p><strong>Conclusion: </strong>Songorine inhibits oxidative stress-related inflammation in sepsis-induced ALI <i>via</i> the activation of the PI3K/AKT/NRF2 signaling pathway.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136397243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T-Cell Metabolism in Rheumatoid Arthritis: Focus on Mitochondrial and Lysosomal Dysfunction","authors":"Asmita Parab, Lokesh Kumar Bhatt","doi":"10.1080/08923973.2024.2330645","DOIUrl":"https://doi.org/10.1080/08923973.2024.2330645","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by immune cell dysregulation, synovial hyperplasia, and progressive cartilage destruction. The loss of immunological self-t...","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140117481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory effect of vitamin D supplementation on Behçet's disease patients: effect on nitric oxide and Th17/Treg cytokines production.","authors":"Randa Oubouchou, Zineb Ait Arab -Djeraba, Yassmine Kemikem, Fifi Otmani, Chafia Touil-Boukoffa","doi":"10.1080/08923973.2023.2239490","DOIUrl":"10.1080/08923973.2023.2239490","url":null,"abstract":"<p><strong>Introduction: </strong>In the last decade, an immuno-modulatory effect of vitamin D supplementation have emerged as a potential therapeutic approach for some inflammatory and autoimmune diseases. As previously reported, vitamin D deficiency was strongly linked to several diseases as Behçet's disease (BD). BD is a chronic systemic inflammatory disorder with autoimmunity, genetic and environmental factors involvement. The aim of our current study is to set up a new therapeutic strategy in BD, combining conventional therapy and vitamin D supplementation.</p><p><strong>Materials and methods: </strong>Blood samples were collected from active and inactive BD patients and healthy controls (HC) to evaluate 25(OH) vitamin D levels using an electrochemiluminescence method. All deficient and insufficient vitamin D BD patients' were supplemented with vitamin D3 (CHOLECALCIFEROL, 200 000 UI/1 ml). In this context, NO, IL-17A and IL-10 levels were evaluated in patients and HC <i>in vivo</i> and <i>ex vivo</i> using Griess and ELISA methods respectively.</p><p><strong>Results: </strong>Before supplementation, we noted with interest that BD patients had vitamin D deficiency, associated with elevated <i>in vivo</i> and <i>ex vivo</i> NO and IL-17A levels compared to HC. Conversely, low IL-10 levels were observed in the same BD patients in comparison to HC. Interestingly, restored vitamin D status in supplemented BD patients was related to the decreased NO levels. In the same way, the IL-10/IL-17A ratio was improved.</p><p><strong>Conclusions: </strong>Collectively, our data suggest that vitamin D supplementation in combination with conventional treatments has a beneficial effect and could constitute a good therapeutic candidate for alleviating inflammatory responses during Behçet disease.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9924435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vinpocetine mitigates methotrexate-induced duodenal intoxication by modulating NF-κB, JAK1/STAT-3, and RIPK1/RIPK3/MLKL signals.","authors":"Hanaa M Tashkandi, Hanan S Althagafy, Fatima A Jaber, Turki Alamri, Nouf S Al-Abbas, Nehad A Shaer, Steve Harakeh, Emad H M Hassanein","doi":"10.1080/08923973.2023.2239491","DOIUrl":"10.1080/08923973.2023.2239491","url":null,"abstract":"<p><strong>Objectives: </strong>Methotrexate (MTX) is an antimetabolite agent widely used to manage a variety of tumors and autoimmune diseases. Nonetheless, MTX-induced intestinal intoxication is a serious adverse effect limiting its clinical utility. Inflammation and oxidative stress are possible mechanisms for MTX-induced intestinal toxicity. Vinpocetine (VNP) is a derivative of the alkaloid vincamine with potent anti-inflammatory and antioxidant effects. The current study investigated the protective intestinal impact of VNP in attenuating MTX-induced intestinal intoxication in rats.</p><p><strong>Materials and methods: </strong>VNP was administered orally in a dose of 20 mg/kg, while MTX was injected intraperitoneal in a dose of 20 mg/kg.</p><p><strong>Results: </strong>VNP administration attenuated drastic histological changes induced by MTX and preserved both normal villus and crypt histology. VNP significantly attenuated oxidative injury by upregulating intestinal Nrf2 and HO-1 expression. VNP attenuated inflammation by reducing MPO, NO₂^-, TNF-α, and IL-1β levels mediated by downregulating NF-κB, NDAPH-oxidase, IRF3, p-JAK-1, and p-STAT-3 expressions. Moreover, VNP potently counteracted intestinal necroptosis by effectively downregulating RIPK1, RIPK3, MLKL, and caspase-8 proteins.</p><p><strong>Conclusion: </strong>Therefore, VNP may represent a promising approach that can attenuate intestinal toxicity in patients receiving MTX.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9927201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Withaferin A suppressed hepatocellular carcinoma progression through inducing IGF2BP3/FOXO1/JAK2/STAT3 pathway-mediated ROS production.","authors":"Jinhai Li, Mengchen Ge, Pengcheng Deng, Xinquan Wu, Longqing Shi, Yu Yang","doi":"10.1080/08923973.2023.2247552","DOIUrl":"10.1080/08923973.2023.2247552","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the underlying molecular mechanisms of Withaferin A (WA) in hepatocellular carcinoma (HCC).</p><p><strong>Materials and methods: </strong>The gene and protein expression were analyzed using RT-qPCR and western blot, respectively. The proliferation of HCC cells was evaluated by CCK-8 assays. The migrative ability of HCC cells was measured by transwell assays.</p><p><strong>Results: </strong>We revealed that WA suppressed the proliferation and migration of HCC cells and inhibited IGF2BP3 (insulin like growth factor 2 mRNA binding protein 3) expression. IGF2BP3 abundance reversed the reactive oxygen species (ROS) accumulation and suppression of HCC cell proliferation and migration induced by WA. Besides, IGF2BP3 suppressed ROS production to promote the growth and migration of HCC cells. Furthermore, we found that IGF2BP3 exerted its tumor-promotive and ROS-suppressive effect on HCC cells by regulating the expression of FOXO1 (forkhead box O1). In addition, IGF2BP3-stimulated activation of JAK2 (Janus kinase 2)/STAT3 (signal transducer and activator of transcription 3) phosphorylation effectively decreased the transcription of FOXO1. FOXO1 abundance decreased the phosphorylation of JAK2 and STAT3 by increasing ROS level, forming a feedback loop for the inhibition of JAK2/STAT3 signaling activated by IGF2BP3.</p><p><strong>Conclusions: </strong>WA-induced ROS inhibited HCC cell growth and migration through the inhibition of IGF2BP3 to deactivate JAK2/STAT3 signaling, resulting in increased FOXO1 expression to further stimulate ROS production and inhibit JAK2/STAT3 signaling.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10159772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Icariin decreases cell proliferation and inflammation of rheumatoid arthritis-fibroblast like synoviocytes via GAREM1/MAPK signaling pathway.","authors":"Zhiming Wu, Qin Liu, Zhengliu Cao, Hui Li, Yifen Zhou, Peng Zhang","doi":"10.1080/08923973.2023.2253990","DOIUrl":"10.1080/08923973.2023.2253990","url":null,"abstract":"<p><strong>Objective: </strong>Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation and joint damage, leading to pain and reduced joint function. Icariin, a flavonoid compound, has been studied for its potential therapeutic role in RA due to its anti-inflammatory and anti-proliferative effects. Here, we aimed to investigate the action mechanism of icariin in regulating RA.</p><p><strong>Materials and methods: </strong>Fibroblast-like synoviocytes (FLS) were obtained from RA and trauma patients, generating RA-FLS and normal FLS. The cells were treated with varying concentrations of icariin (0, 10, 20, 40, 80 μM). We assessed the effects of icariin on cell proliferation, apoptosis, and levels of inflammatory factors using the CCK-8 assay, flow cytometry, and enzyme-linked immunosorbent assay, qRT-PCR, and western blotting.</p><p><strong>Results: </strong>Icariin treatment had no significant impact on the cell proliferation of normal FLS. However, it dose-dependently repressed cell proliferation, reduced TNF-α, IL-6, and IL-1β levels, and increased apoptosis in RA-FLS. The expression of GAREM1, p-p38, and p-ERK1/2 was upregulated in RA-FLS, which was reversed by icariin treatment. Overexpression of GAREM1 reversed the inhibitory effects of icariin on cell proliferation and inflammatory factor levels in RA-FLS.</p><p><strong>Conclusion: </strong>Our findings suggest that icariin treatment can alleviate the development of RA by reducing cell proliferation and inflammation in RA-FLS through the regulation of the GAREM1/MAPK signaling pathway. These results support the potential of icariin as a therapeutic agent for RA treatment. As icariin is safe and well-tolerated in previous studies, further research is warranted to explore its efficacy in clinical settings.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10135646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}