Folia neuropathologica最新文献

{"title":"MiR-484 promotes the malignant progression of glioma by inhibiting CDKN2A expression.","authors":"Yingrui Gu,&nbsp;Hongbing Lei,&nbsp;Peipei Ma,&nbsp;Yi Chen","doi":"10.5114/fn.2023.130002","DOIUrl":"https://doi.org/10.5114/fn.2023.130002","url":null,"abstract":"<p><strong>Introduction: </strong>Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) is involved in glioma progression, but the specific molecular mechanism of CDKN2A in glioma cell migration and invasion needs to be further explored.</p><p><strong>Material and methods: </strong>Data related to CDKN2A expression and glioma overall survival were obtained from The Cancer Genome Atlas (TCGA) database. Then, CDKN2A expression in glioma tissues/cells or paracancer tissues/astrocytes was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blot. Afterwards, Wound healing, Transwell and tube formation assay were performed to identify the invasion, migration and angiogenesis of glioma cells, respectively. TargetScan database predicted the targeted binding between miR-484 and CDKN2A, which was verified by dual luciferase reporter gene assay. Western blot and qRT-PCR were performed to detect the expression of VEGF, E-cadherin, N-cadherin and Vimentin in glioma cells.</p><p><strong>Results: </strong>CDKN2A was low-expressed in glioma tissue/cells as compared to paracancer tissue/astrocytes, and was strongly associated to the poor prognosis of glioma. Further studies found that down-regulation of CDKN2A could promote migration, invasion and angiogenesis of glioma cells. Besides, miR-484 was high-expressed in glioma cells compared to astrocytes. Up-regulation of miR-484 could enhance migration, invasion and angiogenesis of glioma cells. In addition, up-regulated miR-484 suppressed the expression of E-cadherin, and promoted the expression of N-cadherin, Vimentin and VEGF. However, there was negative regulation of miR-484 and CDKN2A, and CDKN2A could partially offset the effect of miR-484.</p><p><strong>Conclusions: </strong>MiR-484 promoted cell migration, invasion and angiogenesis by inhibiting CDKN2A expression.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 3","pages":"249-265"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41196292","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":"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor","authors":"Yuhao Peng, Xiaoling Hu, Haifeng He, Xinting Zhou, Zhonghui Luo","doi":"10.5114/fn.2023.131556","DOIUrl":"https://doi.org/10.5114/fn.2023.131556","url":null,"abstract":"AMA Peng Y, Hu X, He H, Zhou X, Luo Z. Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131556. APA Peng, Y., Hu, X., He, H., Zhou, X., & Luo, Z. (2023). Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131556 Chicago Peng, Yuhao, Xiaoling Hu, Haifeng He, Xinting Zhou, and Zhonghui Luo. 2023. \"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor\". Folia Neuropathologica. doi:10.5114/fn.2023.131556. Harvard Peng, Y., Hu, X., He, H., Zhou, X., and Luo, Z. (2023). Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131556 MLA Peng, Yuhao et al. \"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131556. Vancouver Peng Y, Hu X, He H, Zhou X, Luo Z. Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131556.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"47 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136302706","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":"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway","authors":"Yuan Gao, Jiang Liu, Xiaoyan Wang, Qiang Meng","doi":"10.5114/fn.2023.131191","DOIUrl":"https://doi.org/10.5114/fn.2023.131191","url":null,"abstract":"AMA Gao Y, Liu J, Wang X, Meng Q. Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131191. APA Gao, Y., Liu, J., Wang, X., & Meng, Q. (2023). Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131191 Chicago Gao, Yuan, Jiang Liu, Xiaoyan Wang, and Qiang Meng. 2023. \"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway\". Folia Neuropathologica. doi:10.5114/fn.2023.131191. Harvard Gao, Y., Liu, J., Wang, X., and Meng, Q. (2023). Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131191 MLA Gao, Yuan et al. \"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131191. Vancouver Gao Y, Liu J, Wang X, Meng Q. Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131191.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"96 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135496322","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":"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours","authors":"Michał Sobstyl, Ewa Nagańska, Piotr Glinka, Teresa Wierzba-Bobrowicz, Albert Acewicz, Aleksandra Kuls-Oszmaniec","doi":"10.5114/fn.2023.131640","DOIUrl":"https://doi.org/10.5114/fn.2023.131640","url":null,"abstract":"AMA Sobstyl M, Nagańska E, Glinka P, Wierzba-Bobrowicz T, Acewicz A, Kuls-Oszmaniec A. Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131640. APA Sobstyl, M., Nagańska, E., Glinka, P., Wierzba-Bobrowicz, T., Acewicz, A., & Kuls-Oszmaniec, A. (2023). Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131640 Chicago Sobstyl, Michał, Ewa Nagańska, Piotr Glinka, Teresa Wierzba-Bobrowicz, Albert Acewicz, and Aleksandra Kuls-Oszmaniec. 2023. \"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours\". Folia Neuropathologica. doi:10.5114/fn.2023.131640. Harvard Sobstyl, M., Nagańska, E., Glinka, P., Wierzba-Bobrowicz, T., Acewicz, A., and Kuls-Oszmaniec, A. (2023). Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131640 MLA Sobstyl, Michał et al. \"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131640. Vancouver Sobstyl M, Nagańska E, Glinka P, Wierzba-Bobrowicz T, Acewicz A, Kuls-Oszmaniec A. Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131640.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"37 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136007887","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":"LINC00470 represses cell autophagy and cisplatin sensitivity of glioma via suppressing PTEN expression.","authors":"Biyin Chen,&nbsp;Wenwu Wang,&nbsp;Fangfeng Lin,&nbsp;Shuping Shi,&nbsp;Shunjie Ou,&nbsp;Yunqiu Yu","doi":"10.5114/fn.2023.125327","DOIUrl":"https://doi.org/10.5114/fn.2023.125327","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma is one of primary brain tumours which has the worst clinical prognoses of patients. As an alternative chemotherapeutic drug for malignant glioma, the therapeutic effect of cisplatin (CDDP) is devastatingly affected due to resistance in patients. In this study, we investigated the effect of LINC00470/PTEN on the CDDP sensitivity of glioma cells.</p><p><strong>Material and methods: </strong>Differentially expressed lncRNAs and the downstream regulators in glioma tissue were obtained via bioinformatics analysis. LINC00470 and PTEN mRNA expression levels were detected using qRT-PCR. IC50 values of glioma cells were examined using Cell Counting Kit-8 (CCK-8). Cell apoptosis was revealed by flow cytometry. The expression level of autophagy-related protein was detected by western blot. Intracellular autophagosome formation was detected by immunofluorescence staining, and the methylation level of PTEN promoter was detected via methylation-specific PCR (MSP).</p><p><strong>Results: </strong>Through the above steps, we found that LINC00470 was highly expressed in glioma cells, and the survival rate of patients was reduced in the presence of high expression of LINC00470. Silenced LINC00470 promoted LC3 II expression and autophagosome formation, and facilitated cell apoptosis to inhibit resistance to CDDP. While silenced PTEN could successfully reverse the previous effects on glioma cells.</p><p><strong>Conclusions: </strong>Based on the above, LINC00470 repressed cell autophagy by constraining PTEN, thereby enhancing CDDP resistance of glioma cells.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 1","pages":"88-96"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9398471","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":"Upregulated lncRNA NORAD can diagnose acute cerebral ischemic stroke patients and predict poor prognosis.","authors":"Dongliang Liu,&nbsp;Li Li,&nbsp;Juanjuan Xu,&nbsp;Wenping Luo,&nbsp;Lu Pan,&nbsp;Qilin Niu,&nbsp;Daoxiang Wei","doi":"10.5114/fn.2022.121478","DOIUrl":"https://doi.org/10.5114/fn.2022.121478","url":null,"abstract":"<p><strong>Introduction: </strong>Acute cerebral ischemic stroke (AIS) dramatically influences patients' quality of life. lncRNA NORAD (NORAD) has been studied in cerebrovascular diseases, which are potential risk factors for AIS. The specific significance of NORAD is unclear. This study aimed to assess the role of NORAD in AIS, and to provide therapeutic value for its' treatment.</p><p><strong>Material and methods: </strong>A total of 103 AIS patients and 95 healthy individuals (control) were enrolled into this study. Expression level of NORAD in the plasma of all participants was analyzed by PCR. Diagnostic potential of NORAD in AIS was evaluated by ROC analysis, while Kaplan-Meier and Cox regression analyses were conducted to assess its' prognostic value in AIS.</p><p><strong>Results: </strong>A significantly increased level of NORAD was observed in AIS patients compared with healthy individuals. The upregulation of NORAD could dramatically discriminate AIS patients from healthy individuals with high sensitivity (81.60%) and specificity (88.40%). NORAD was positively correlated with patients' high-sensitivity C-reactive protein (hs CRP, r = 0.796), matrix metalloproteinase-9 (MMP9, r = 0.757), and NIHSS scores ( r = 0.840), and negatively related to pc-ASPECTS scores ( r = -0.607). Moreover, NORAD upregulation was associated with patients' unfavorable prognosis and served as an independent prognostic biomarker, together with NIHSS and pc-ASPECTS scores of AIS patients.</p><p><strong>Conclusions: </strong>NORAD was upregulated in AIS, which can discriminate AIS patients, and was closely correlated with severe development and poor prognosis of patients.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 1","pages":"105-110"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9727309","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":"ADAMTS8 inhibits glioma development in vitro and in vivo.","authors":"Baosheng Zhou,&nbsp;Yong Liu,&nbsp;Guangshuo Ma,&nbsp;Xiuyu Wang,&nbsp;Binge Chang,&nbsp;Hongwei Lu,&nbsp;Xuequan Feng","doi":"10.5114/fn.2023.129380","DOIUrl":"https://doi.org/10.5114/fn.2023.129380","url":null,"abstract":"<p><strong>Introduction: </strong>In recent years, novel RNAs have been revealed to be regulators in glioma. ADAMTS8 has been reported to be reduced in brain tumours. In this study, we aimed to explore the role of ADAMTS8 in glioma.</p><p><strong>Material and methods: </strong>Online bioinformatic tools, Gepia and Chinese Glioma Genome Atlas database (CGGA) were used to analyse the differential expression of ADAMTS8, overall survival and disease-free survival rates and the correlations between ADAMTS8 and matrix metallopeptidases (MMP2 and MMP9) in glioma. RT-qPCR and western blot experiments were performed to measure the mRNA and protein expression. ADAMTS8 expression was regulated in cells through transfection. Thereafter, the effect of ADAMTS8 on cells was investigated through the cell viability, apoptosis and transwell experiments. The epithelial-mesenchymal transition (EMT)-related proteins and also MMP2 and MMP9 were examined. The subcutaneous tumour model was established to validate the suppressive role of ADAMTS8 in tumour growth.</p><p><strong>Results: </strong>ADAMTS8 expression was reduced in glioma tissues and cells. Higher expression of ADAMTS8 was correlated with higher survival rates. ADAMTS8 was correlated with MMP2 and MMP9 in glioma tissues. In glioma cells, overexpression of ADAMTS8 could inhibit the viability, invasion, migration and EMT, and MMP2 and MMP9, but promote the apoptosis of cells. The upregulation of ADAMTS8 could inhibit the tumour growth in vivo.</p><p><strong>Conclusions: </strong>ADAMTS8 was inhibited in glioma and the higher expression of ADAMTS8 might be related to better prognosis among glioma patients. Overexpression of ADAMTS8 inhibited the development of glioma in vitro and in vivo.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 2","pages":"144-152"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10022088","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 chemotherapies on the crosstalk interaction between CD8 cytotoxic T-cells and MHC-I peptides in the microenvironment of WHO grade 4 astrocytoma.","authors":"Nadeem Butt,&nbsp;Maryam Enani,&nbsp;Maryam Alshanqiti,&nbsp;Alaa Alkhotani,&nbsp;Taghreed Alsinani,&nbsp;Mohammed Matoog Karami,&nbsp;Motaz M Fadul,&nbsp;Majid Almansouri,&nbsp;Amber Hassan,&nbsp;Saleh Baeesa,&nbsp;Ahmed K Bamaga,&nbsp;Shadi Alkhayyat,&nbsp;Eyad Faizo,&nbsp;Maher Kurdi","doi":"10.5114/fn.2023.131014","DOIUrl":"https://doi.org/10.5114/fn.2023.131014","url":null,"abstract":"<p><strong>Introduction: </strong>CD8 + T-cells and MHC-I have been detected in brain gliomas with a significant outcome. The effect of chemotherapies on the crosstalk interaction between CD8 + T-cells and MHC-I has never been explored.</p><p><strong>Material and methods: </strong>The protein expression profiling of CD8 cytotoxic T-cells and the gene expression assay of MHC-I in 35 patients diagnosed with WHO grade 4 astrocytoma were performed. The impact of these two factors on tumor recurrence was analyzed.</p><p><strong>Results: </strong>IDH was wildtype in 13 tumors. MHC-I protein expression was absent or low in 34 tumors and dense in a single case. MHC-I gene expression was upregulated in 10 tumors and 25 tumors showed MHC-I gene downregulation. Temozolomide (TMZ) was given to 24 patients and 11 patients received TMZ plus other chemotherapies. No statistically significant association was observed between IDH mutation and CD8 + T-cells ( p = 0.383). However, this association was significant in recurrence-free interval (RFI) ( p = 0.012). IDH-wildtype tumors with highly infiltrated CD8 + T-cells or IDH-mutant tumors with low CD8 + T-cells showed late tumor recurrence. There was a statistically significant difference in RFI between tumors with different MHC-I expression and CD8 + T-cell counts after treatment with TMZ or TMZ plus ( p = 0.026).</p><p><strong>Conclusions: </strong>No association between IDH mutation and CD8+ cytotoxic T-cell was found. IDH is directly linked to tumor recurrence regardless of CD8 + T-cells infiltration. TMZ plus other adjuvants is proved to be more effective in improving patient survival and delaying tumor recurrence, as compared to using TMZ alone. Nonetheless, none-TMZ adjuvants may increase tumor sensitization to cytotoxic T-cells more than TMZ.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 3","pages":"317-325"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41196296","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":"Exercise attenuates mitochondrial autophagy and neuronal degeneration in MPTP induced Parkinson's disease by regulating inflammatory pathway.","authors":"Zhiwei Li, Hua Lv, Xiaoli Cui, Wei Di, Xiansong Cheng, Jun Liu, Alok Tripathi","doi":"10.5114/fn.2023.132424","DOIUrl":"10.5114/fn.2023.132424","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a chronic neuronal loss of dopamine and drugs used for its management has several limitations. The present report determines the effect of exercise on mitochondrial autophagy against PD. Parkinson's disease was induced by 15 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg, i.p.) for 3 weeks, on five consecutive days in a week. Exposure of exercise was provided for 40 min for a period of 2 weeks after PD confirmation. Assessment of behaviour was performed to evaluate the effect of exercise on motor function and cognitive function in PD rats. Levels of reactive oxygen species (ROS) and inflammatory cytokines were assessed in PD rats using enzyme linked immunosorbent assay (ELISA). Expression of myocyte-specific enhancer factor 2D (MEF2D) and NADH dehydrogenase 6 (ND6) was estimated in PD rats. Exposure to exercise ameliorates the altered motor function and cognitive function in PD rats. There was a reduction in ROS and cytokine levels in the brain tissue of the exercise group compared to the negative control group. Exercise ameliorates the altered expression of apoptotic proteins and mRNA expression of MEF2D and ND6 in the brain tissue of MPTP induced PD rats. In conclusion, data of study reveal that exercise protects the mitochondrial autophagy in PD rats by reducing inflammatory cytokines and oxidative stress.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"426-432"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086556","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":"PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage","authors":"Na Hu, Ran An, Kun Yu, Yanzhong Chang, Weijuan Gao","doi":"10.5114/fn.2023.130449","DOIUrl":"https://doi.org/10.5114/fn.2023.130449","url":null,"abstract":"AMA Hu N, An R, Yu K, Chang Y, Gao W. PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.130449. APA Hu, N., An, R., Yu, K., Chang, Y., & Gao, W. (2023). PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.130449 Chicago Hu, Na, Ran An, Kun Yu, Yanzhong Chang, and Weijuan Gao. 2023. \"PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage\". Folia Neuropathologica. doi:10.5114/fn.2023.130449. Harvard Hu, N., An, R., Yu, K., Chang, Y., and Gao, W. (2023). PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.130449 MLA Hu, Na et al. \"PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.130449. Vancouver Hu N, An R, Yu K, Chang Y, Gao W. PF4 induces inflammatory response through NF-kB signal pathway in rats with intracerebral haemorrhage. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.130449.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"135 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136007874","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}