International Journal of Immunopathology and Pharmacology最新文献

{"title":"Retinol dehydrogenase 10 promotes epithelial-mesenchymal transition in spinal cord gliomas via PI3K/AKT pathway.","authors":"Zijun Zhao, Zihan Song, Zairan Wang, Fan Zhang, Ze Ding, Zongmao Zhao, Liqiang Liu, Tao Fan","doi":"10.1177/03946320241276336","DOIUrl":"10.1177/03946320241276336","url":null,"abstract":"<p><p><b>Background:</b> Spinal cord glioma (SCG), a rare subset of central nervous system (CNS) glioma, represents a complex challenge in neuro-oncology. There has been research showing that Retinol Dehydrogenase 10 (RDH10) may be a tumor promoting factor in brain glioma, but the biological effects of RDH10 remain undefined in SCG. <b>Methods:</b> We performed gene set enrichment analysis (GSEA) and unsupervised clustering analysis to investigate the roles of EMT (epithelial-mesenchymal transition) in glioma. DEG (differently expressed gene) screening and correlation analysis were conducted to filter the candidate genes which were closely associated with EMT process in SCG. Enrichment analysis and GSVA (Gene Set Variation Analysis) were conducted to investigate the potential mechanism of RDH10 for SCG. Trans-well and healing assay were performed to explore the role of RDH10 in the invasion of SCG. Western blotting was performed to evaluate the levels of markers in PI3K-AKT and EMT pathway. In vivo tests were conducted to verify the role of RDH10 in EMT process. <b>Results:</b> Bioinformatic analysis demonstrated the EMT pathway was associated with dismal prognosis of glioma. Further analysis demonstrated that RDH10 showed the strongest correlation with the EMT process. Retinol Dehydrogenase 10 expression was significantly increased in SCG tissues, correlating with advanced tumor grade and unfavorable prognosis. Functional analysis indicated that decreasing RDH10 levels impeded the invasive and migratory abilities of SCG cells, whereas increasing RDH10 levels augmented them. Enrichment analysis and western blot revealed that RDH10 regulated EMT process of SCG by PI3K-AKT pathway. We observed that the enhanced invasion ability and increased EMT-related protein induced by RDH10 overexpression can be suppressed by PI3K-AKT pathway inhibitor (LY294002). <b>Conclusion:</b> Our research found that RDH10 was an effective biomarker associated with tumor grade and prognosis of SCG. RDH10 could regulate EMT process of SCG through PI3K-AKT pathway.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241276336"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11344904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047351","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":"Protocatechuic aldehyde attenuates chondrocyte senescence via the regulation of PTEN-induced kinase 1/Parkin-mediated mitochondrial autophagy.","authors":"Lishi Jie, Xiaoqing Shi, Junfeng Kang, Houyu Fu, Likai Yu, Di Tian, Wei Mei, Songjiang Yin","doi":"10.1177/03946320241271724","DOIUrl":"10.1177/03946320241271724","url":null,"abstract":"<p><p>This study aimed to investigate whether the beneficial effects of PCA on chondrocyte senescence are mediated through the regulation of mitophagy. Chondrocyte senescence plays a significant role in the development and progression of knee osteoarthritis (OA). The compound protocatechuic aldehyde (PCA), which is abundant in the roots of <i>Salvia miltiorrhiza</i>, has been reported to have antioxidant properties and the ability to protect against cellular senescence. To achieve this goal, a destabilization of the medial meniscus (DMM)-induced mouse OA model and a lipopolysaccharide (LPS)-induced chondrocyte senescence model were used, in combination with PINK1 gene knockdown or overexpression. After treatment with PCA, cellular senescence was assessed using Senescence-Associated β-Galactosidase (SA-β-Gal) staining, DNA damage was evaluated using Hosphorylation of the Ser-139 (γH2AX) staining, reactive oxygen species (ROS) levels were measured using Dichlorodihydrofluorescein diacetate (DCFH-DA) staining, mitochondrial membrane potential was determined using a 5,5',6,6'-TETRACHLORO-1,1',3,3'-*. TETRAETHYBENZIMIDA (JC-1) kit, and mitochondrial autophagy was examined using Mitophagy staining. Western blot analysis was also performed to detect changes in senescence-related proteins, PINK1/Parkin pathway proteins, and mitophagy-related proteins. Our results demonstrated that PCA effectively reduced chondrocyte senescence, increased the mitochondrial membrane potential, facilitated mitochondrial autophagy, and upregulated the PINK1/Parkin pathway. Furthermore, silencing PINK1 weakened the protective effects of PCA, whereas PINK1 overexpression enhanced the effects of PCA on LPS-induced chondrocytes. PCA attenuates chondrocyte senescence by regulating PINK1/Parkin-mediated mitochondrial autophagy, ultimately reducing cartilage degeneration.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241271724"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11311163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908055","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":"Corrigendum to \"Bibliometric and visual analyses of trends in the field of T cell exhaustion research: Findings from 2000 to 2022\".","authors":"","doi":"10.1177/03946320241226506","DOIUrl":"10.1177/03946320241226506","url":null,"abstract":"","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241226506"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10804896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513920","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":"Evaluation of the protective effect of coenzyme Q₁₀ on hepatotoxicity caused by acute phosphine poisoning.","authors":"Mohammad Reza Hooshangi Shayesteh, Zahra Hami, Mohsen Chamanara, Mohammad Reza Parvizi, Alireza Golaghaei, Ehsan Nassireslami","doi":"10.1177/03946320241250286","DOIUrl":"10.1177/03946320241250286","url":null,"abstract":"<p><p><i>Background</i>: Aluminum phosphide (AlP) poisoning is prevalent in numerous countries, resulting in high mortality rates. Phosphine gas, the primary agent responsible for AlP poisoning, exerts detrimental effects on various organs, notably the heart, liver and kidneys. Numerous studies have documented the advantageous impact of Coenzyme Q₁₀ (CoQ₁₀) in mitigating hepatic injuries. The objective of this investigation is to explore the potential protective efficacy of CoQ₁₀ against hepatic toxicity arising from AlP poisoning. <i>Method</i>: The study encompassed distinct groups receiving almond oil, normal saline, exclusive CoQ₁₀ (at a dosage of 100 mg/kg), AlP at 12 mg/kg; LD₅₀ (lethal dose for 50%), and four groups subjected to AlP along with CoQ₁₀ administration (post-AlP gavage). CoQ₁₀ was administered at 10, 50, and 100 mg/kg doses via Intraparietal (ip) injections. After 24 h, liver tissue specimens were scrutinized for mitochondrial complex activities, oxidative stress parameters, and apoptosis as well as biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT). <i>Results</i>: AlP induced a significant decrease in the activity of mitochondrial complexes I and IV, as well as a reduction in catalase activity, Ferric Reducing Antioxidant Power (FRAP), and Thiol levels. Additionally, AlP significantly elevated oxidative stress levels, indicated by elevated reactive oxygen species (ROS) production, and resulted in the increment of hepatic biomarkers such as AST and ALT. Administration of CoQ₁₀ led to a substantial improvement in the aforementioned biochemical markers. Furthermore, phosphine exposure resulted in a significant reduction in viable hepatocytes and an increase in apoptosis. Co-treatment with CoQ₁₀ exhibited a dose-dependent reversal of these observed alterations. <i>Conclusion</i>: CoQ₁₀ preserved mitochondrial function, consequently mitigating oxidative damage. This preventive action impeded the progression of heart cells toward apoptosis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241250286"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065768","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":"Phillygenin rescues impaired autophagy flux by modulating the PI3K/Akt/mToR signaling pathway in a rat model of severe acute pancreatitis.","authors":"Jiaxing Li, Jiming Duan, Yiwen Sun, Ruifeng Yang, Hong Yang, Wenxing Li","doi":"10.1177/03946320241309260","DOIUrl":"10.1177/03946320241309260","url":null,"abstract":"<p><p>To investigate the mechanism of pancreatic alveolar cell autophagy in rats with severe acute pancreatitis (SAP) by phillygenin (PHI) based on the PI3K/Akt/mToR pathway. Rats were randomly divided into control group (CON group), SAP model group (SAP group) and PHI treatment group (SAP+PHI group), with 10 rats in each group. 5% sodium taurocholate was injected retrogradely into the biliopancreatic duct to establish a SAP rat model, and PHI was injected intraperitoneally into the pancreas after successful establishment of the model. The colorimetric assay was used to determine serum amylase and lipase activity levels. Pancreatic morphology and histological changes were assessed by H&E staining. Autophagy-related indices were determined by immunohistochemistry: LC3-II, P62, LAMP. Autophagy pathway-related indices were determined by western blotting assay: p-PI3K, PI3K, p-Akt, Akt, p-mToR, mToR. Autophagy vesicle alteration. Compared with the SAP group, the SAP+PHI group showed a decrease in amylase, lipase and pathological score, an increase in the expression of LAMP-2, and a decrease in the expression of p62, p-PI3K, p-Akt and p-mToR, with a statistically significant difference (<i>p</i> < 0.05). Electron microscopy showed that autophagic flux was restored and accumulated autophagic vehicles were relatively reduced by PHI intervention. PHI can rescue the impaired autophagic flux by inhibiting the PI3K/Akt/mToR pathway, allowing abnormal autophagic vesicles to complete autophagy to protect the rat.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241309260"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142839863","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":"Study of the possible effect of sacubitril/valsartan combination versus valsartan on the cognitive function in Alzheimer's disease model in rats.","authors":"Abdallah Salah El-Din Hussein,&nbsp;Rahma Kamal El-Din Abou-El Nour,&nbsp;Omayma A Khorshid,&nbsp;Afaf S Osman","doi":"10.1177/03946320231161469","DOIUrl":"https://doi.org/10.1177/03946320231161469","url":null,"abstract":"<p><p><b>Objectives:</b> Alzheimer's disease (AD) is an irreversible, progressive neurodegenerative disorder. The proportion of elderly individuals at risk for AD and cardiovascular problems increases by raising life expectancy. The present study was designed to investigate the effect of the sacubitril/valsartan combination compared to that of valsartan alone in a rat model of AD. <b>Methods:</b> 72 male adult Wistar rats were divided into seven groups; control untreated rats received saline, control valsartan-treated rats received valsartan orally, control sacubitril/valsartan treated rats received sacubitril/valsartan orally, model rats received aluminum chloride i.p., model valsartan treated rats received aluminum chloride i.p. and valsartan orally and model sacubitril/valsartan treated rats received aluminum chloride i.p. and sacubitril/valsartan combination orally. All previous treatments continued on a daily basis for 6 weeks. At the second, fourth, and sixth weeks of the experiment, behavioral changes were evaluated using the Morris water maze and novel object recognition tests, and systolic blood pressure was measured. In the end, rat brain malondialdehyde and amyloid-beta 1-42 levels were measured, and the isolated hippocampus was evaluated histopathologically. <b>Results:</b> Valsartan improved AD symptoms in the aluminum-induced rat model, while the sacubitril/valsartan combination significantly worsened all tested parameters in both control and model rats compared with untreated and valsartan-treated animals. <b>Conclusion:</b> Based on the current study's findings, valsartan did not increase the risk for AD development in control rats and improved AD symptoms in a rat model, while sacubitril/valsartan combination increased the risk of AD in control rats and worsened the condition in a rat model.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231161469"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ee/17/10.1177_03946320231161469.PMC9996744.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9085070","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":"Down-regulation of S1PR2 is correlated with poor prognosis and immune infiltrates in cervical squamous cell carcinoma and endocervical adenocarcinoma.","authors":"Yu Zhang,&nbsp;Haichuan Wang,&nbsp;Jie Lu,&nbsp;Qiang Lv,&nbsp;Bei Yun,&nbsp;Zhiru Ge,&nbsp;Li Yan","doi":"10.1177/03946320231178131","DOIUrl":"10.1177/03946320231178131","url":null,"abstract":"<p><p><b>Objectives:</b> Cervical squamous cell carcinoma and cervical adenocarcinoma (CESC) are the second leading cause of deaths from malignant tumors in women, while their therapeutic and diagnostic aims are still finited. A growing body of evidence indicated that sphingosine-1-phosphate receptor 2 (S1PR2) plays essential roles in the occurrence and development about several human cancers. Nevertheless, the key mechanism and role mechanism of S1PR2 in CESC are still unclear.<b>Methods:</b> We first used Tissue Expression (GTEx) and Genotypic Cancer Genome Atlas (TCGA) data to perform pan-cancer analysis on the expression and prognosis of S1PR2, and found that S1PR2 may have a potential impact on CESC. To generate a protein-protein interaction (PPI) network using the STRING database. The clusterProfiler package is used for feature-rich analysis. The Tumor IMmune Estimation Resource was used to determine the connection between S1PR2 mRNA expression and immune infiltrates. <b>Results:</b> S1PR2 expression in CESC tissues was down-regulated compared with adjacent normal tissues. Kaplan-Meier analysis indicated that compared with patients with high expression of S1PR2, CESC patients with low S1PR2 expression had a worse prognosis. Reduced S1PR2 expression is associated with patients with high clinical stage, more histological types of squamous cell carcinoma, and poor primary treatment outcomes. The receiver operating characteristic curve of S1PR2 was 0.870. Correlation analysis showed that the mRNA expression of S1PR2 was related to immune infiltrates and tumor purity.<b>Conclusion:</b> Down-regulated S1PR2 expression is related to poor survival and immune infiltration in CESC. S1PR2 is a potential biomarker for poor prognosis and as a potential target for CESC immune therapy.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231178131"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4e/e8/10.1177_03946320231178131.PMC10226337.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9915889","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":"Immune system modulation by low-dose ionizing radiation-induced adaptive response.","authors":"Soha M Hussien,&nbsp;Engy R Rashed","doi":"10.1177/03946320231172080","DOIUrl":"https://doi.org/10.1177/03946320231172080","url":null,"abstract":"<p><strong>Objective: </strong>Hormesis or low-dose ionizing radiation is known to induce various biological responses, a subcategory of which is the adaptive response, which has been reported to protect against higher radiation doses via multiple mechanisms. This study investigated the role of the cell-mediated immunological component of low-dose ionizing radiation-induced adaptive response.</p><p><strong>Methods: </strong>Herein, male albino rats were exposed to whole-body gamma radiation, using a Cs¹³⁷ source with low-dose ionizing radiation doses of 0.25 and 0.5 Gray (Gy); 14 days later, another irradiation session at a dose level of 5 Gy was carried on. Four days post-irradiation at 5 Gy, rats were sacrificed. The low-dose ionizing radiation-induced immuno-radiological response has been assessed through the T-cell receptor (TCR) gene expression quantification. Also, the serum levels of each of interleukins-2 and -10 (IL-2, IL-10), transforming growth factor-beta (TGF-β), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were quantified.</p><p><strong>Results: </strong>Results indicated that priming low irradiation doses resulted in significant decrements in TCR gene expression and the serum levels of IL-2, TGF-β, and 8-OHdG with an increment in IL-10 expression compared to the irradiated group, which did not receive low priming doses.</p><p><strong>Conclusion: </strong>The observed low-dose ionizing radiation-induced radio-adaptive response significantly protected against high irradiation dose injuries, through immune suppression, representing a promising pre-clinical protocol that would be applied to minimize radiotherapy side effects on normal but not against the tumor cells.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231172080"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/42/e9/10.1177_03946320231172080.PMC10127215.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9961407","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":"Multiple sclerosing hemangiomas mimicking hepatocellular carcinoma: A case report.","authors":"Xinyu Zhan,&nbsp;Yiyun Gao,&nbsp;Jian Xu,&nbsp;Dongming Wu,&nbsp;Ping Wang,&nbsp;Haoming Zhou","doi":"10.1177/03946320231190898","DOIUrl":"10.1177/03946320231190898","url":null,"abstract":"<p><p>Hepatocellular carcinoma is a prevalent malignant tumor affecting the liver, and surgical resection and liver transplantation are the primary treatment options for early-stage HCC patients. However, the presence of benign hepatic tumors with similar imaging characteristics to HCC poses challenges in diagnosing and treating the disease, often resulting in misdiagnosis and inappropriate treatment. This case report presents a 52-year-old female patient who exhibited space-occupying liver lesions on abdominal CT and MRI scans. Based on pathological sections from other hospitals, liver malignancy was highly suspected, and hepatocellular tumor was diagnosed preoperatively. But the tumor markers of the patient were all within the normal range. After evaluating the overall condition of the patient, we finally chose the diagnosis and treatment of dissection and partial hepatectomy. Surprisingly, the final diagnosis of postoperative pathology was sclerosing hemangioma. The patient recovered well and was discharged 2 weeks later. Hepatic sclerosing hemangioma is an extremely rare disease that can be easily mistaken for malignant liver tumors due to absence of typical imaging presentations. The diagnosis also needs to be differentiated from other benign tumors, such as liver adenoma and liver abscess, according to the medical history, symptoms, and auxiliary examinations. Therefore, special attention should be given to the diagnosis and treatment of sclerosing hemangioma.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231190898"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fc/67/10.1177_03946320231190898.PMC10467195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10126458","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":"Experimental study on the effect of luteolin on the proliferation, apoptosis and expression of inflammation-related mediators in lipopolysaccharide-induced keratinocytes.","authors":"Xinpei Wang,&nbsp;Yue Yao,&nbsp;Yexian Li,&nbsp;Shujing Guo,&nbsp;Yanjia Li,&nbsp;Guoqiang Zhang","doi":"10.1177/03946320231169175","DOIUrl":"https://doi.org/10.1177/03946320231169175","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed at exploring the effects of luteolin on psoriasis-like cell model proliferation, apoptosis regulation and the expression of inflammation-related mediators.</p><p><strong>Methods: </strong>A Cell Counting Kit-8 (CCK-8) assay was used to determine the survival rate of human immortalized keratinocytes (HaCaT cells) and normal human epidermal keratinocytes (NHEK cells) following stimulation with luteolin and lipopolysaccharide (LPS). Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis were used to detect the protein and mRNA expressions of nuclear factor (NF)-κB p65 and interleukin (IL)-6 after LPS stimulation. Then a luteolin stimulation protocol (10 μmol/L, 24 h) was determined and a reasonable LPS stimulation concentration (20 μg/mL, 24 h) was chosen to establish the psoriasis cell model. Keratinocytes in luteolin pre-treatment and control groups were stimulated with 20 μg/mL LPS for 24 h, and the expressions of NF-κB p65 and IL-6 were detected by western blot and RT-qPCR. The apoptosis of HaCaT cells was detected by flow cytometry, and the enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of psoriasis-related inflammatory factors.</p><p><strong>Results: </strong>CCK-8 assay indicated that luteolin inhibited the proliferation of keratinocytes. LPS stimulated the proliferation of keratinocytes and upregulated the expression of NF-κB p65 and IL-6 in a concentration-dependent manner, and induced psoriasis-like changes. Furthermore, the protein and mRNA expression levels of NF-κB p65 and IL-6 were decreased in the luteolin pre-stimulation group (<i>p</i> < 0.05). Treatment with luteolin downregulated the expression of the LPS-induced inflammatory mediators in keratinocytes (<i>p</i> < 0.05). The flow cytometry results showed that luteolin induced HaCaT cells apoptosis. Finally, ELISA results demonstrated that luteolin inhibited the release of the IL-17, IL-23 and tumor necrosis factor α (TNF-α) in the pre-stimulation group (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>This study confirmed that luteolin can effectively relieve inflammatory mediators in LPS-induced keratinocyte models of psoriasis, which suggested the potential of luteolin in treating psoriasis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231169175"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fa/70/10.1177_03946320231169175.PMC10087617.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10167511","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}