International Journal of Experimental Pathology最新文献_第8页

Comparison of topical sucralfate with dexpanthenol in rat wound model 外用硫糖钠与葡聚糖醇在大鼠创伤模型中的比较

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-20 DOI: 10.1111/iep.12441

Eda Yildizhan, Burak Veli Ulger, Murat Akkus, Dilara Akinci, Omer Basol

{"title":"Comparison of topical sucralfate with dexpanthenol in rat wound model","authors":"Eda Yildizhan, Burak Veli Ulger, Murat Akkus, Dilara Akinci, Omer Basol","doi":"10.1111/iep.12441","DOIUrl":"10.1111/iep.12441","url":null,"abstract":"Wound healing is a dynamic process initiated in response to injury. There are many factors that have detrimental effects on the wound healing process. Numerous studies have been conducted for improving wound healing processes. Dexpanthenol is widely used to accelerate wound healing. Sucralfate is used for the treatment of peptic ulcers. We aimed to compare the efficacy of topical Dexpanthenol and Sucralfate in an experimental wound model in rats via histopathological examinations and immune histochemical determinations, as well, to evaluate their effects on EGF levels. Three different groups were formed: the Control Group, the Dexpanthenol Group and the Sucralfate Group. Full-thickness skin wounds were created on the back of each rat and isotonic saline was applied to the wounds of the rats in the control group, Bepanthol® cream was applied in Dexpanthenol Group and 10% Sucralfate cream was applied in Sucralfate Group, once a day. On the 7th, 14th and 21st days the wounds were measured and seven rats from each group were sacrificed and the wounds were excised for histopathological examination. Sucralfate increased wound healing rates by increasing neovascularization, fibroblast activation, reepithelialization and collagen density, as well as dexpanthenol. Our study revealed that the dexpanthenol and sucralfate groups were better than the control group in terms of their effects on wound healing, however there was no statistically significant difference among these two groups. Sucralfate improves EGF expression in skin wounds and has positive results on skin wound healing comparable to dexpanthenol.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 4","pages":"164-170"},"PeriodicalIF":3.0,"publicationDate":"2022-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9910390","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}

引用次数: 1

Correlations between histological characterizations and methylation statuses of tumour suppressor genes in Wilms' tumours Wilms肿瘤中肿瘤抑制基因的组织学特征与甲基化状态之间的相关性

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-18 DOI: 10.1111/iep.12442

Yen-Chein Lai, Meng-Yao Lu, Wen-Chung Wang, Tai-Cheng Hou, Chen-Yun Kuo

{"title":"Correlations between histological characterizations and methylation statuses of tumour suppressor genes in Wilms' tumours","authors":"Yen-Chein Lai, Meng-Yao Lu, Wen-Chung Wang, Tai-Cheng Hou, Chen-Yun Kuo","doi":"10.1111/iep.12442","DOIUrl":"10.1111/iep.12442","url":null,"abstract":"Wilms' tumour is a solid tumour that frequently occurs in children. Genetic changes in WT1 and epigenetic aberrations that affect imprinted control region 1 in WT2 loci are implicated in its aetiology. Moreover, tumour suppressor genes are frequently silenced by methylation in this tumour. In the present study, we analysed the methylation statuses of promoter regions of 24 tumour suppressor genes using a methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA)-based approach in 6 Wilms' tumours. Methylation of RASSF1 was specific to all 6 Wilms' tumours and was not observed in normal tissues. Moreover, methylated HIC1 was identified in stromal-type Wilms' tumours and methylated BRCA1 was identified in epithelial-type Wilms' tumours. Unmethylated CASP8, RARB, MLH1_167, APC and CDKN2A were found only in blastemal predominant-type Wilms' tumour. Our results indicated that methylation of RASSF1 may be a vital event in the tumorigenesis of Wilms' tumour, which informs its clinical and therapeutic management. In addition, mixed-type Wilms' tumours may be classified according to epithelial, stromal and blastemal components via MS-MLPA-based approach.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 3","pages":"121-128"},"PeriodicalIF":3.0,"publicationDate":"2022-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9548330","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}

引用次数: 0

lncRNA MIAT targets miR-411-5p/STAT3/PD-L1 axis mediating hepatocellular carcinoma immune response lncRNA MIAT靶向miR-411-5p/STAT3/PD-L1轴介导肝癌免疫应答

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-15 DOI: 10.1111/iep.12440

Xiaoxia Zhang, Banglun Pan, Jiacheng Qiu, Xiaoling Ke, Shuling Shen, Xiaoqian Wang, Nanhong Tang

{"title":"lncRNA MIAT targets miR-411-5p/STAT3/PD-L1 axis mediating hepatocellular carcinoma immune response","authors":"Xiaoxia Zhang, Banglun Pan, Jiacheng Qiu, Xiaoling Ke, Shuling Shen, Xiaoqian Wang, Nanhong Tang","doi":"10.1111/iep.12440","DOIUrl":"10.1111/iep.12440","url":null,"abstract":"Emerging evidences have shown that long noncoding RNA (lncRNA) plays an important role in the immune escape of cancer cells. Our previous study has demonstrated that lncRNA MIAT is associated with the immune infiltration of hepatocellular carcinoma (HCC). However, the underlying mechanism of MIAT regulating the PD-L1-mediated immune escape of HCC is poorly understood. Quantitative real-time PCR (qRT-PCR) was used to detect the expression of MIAT and PD-L1 mRNA in HCC. The relationship between MIAT, miR-411-5p, STAT3 and PD-L1 was explored by dual-luciferase reporter assay, cytotoxicity assay, Western blot and RNA immunoprecipitation (RIP). In addition, the xenograft model was established to determine the effect of MIAT on PD-L1 expression in vivo. We found that MIAT and PD-L1 were significantly upregulated in HCC tissues and the expression of PD-L1 was regulated by MIAT. The knockdown of MIAT enhanced the cytotoxicity of T cells on HCC cells. MIAT negatively regulated miR-411-5p expression, upregulated STAT3 and ultimately increased PD-L1 expression from the transcription level. The inhibition of miR-411-5p reversed STAT3 and PD-L1 expression inhibited by MIAT knockdown in HCC cells. This study suggests a novel lncRNA-mediated mechanism for HCC cells to evade the immune response; MIAT/miR-411-5p/STAT3/PD-L1 may be a novel therapeutic target for HCC.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 3","pages":"102-111"},"PeriodicalIF":3.0,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9559826","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}

引用次数: 8

High level of FHL2 exacerbates the outcome of non-small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells 高水平的FHL2加剧了非小细胞肺癌(NSCLC)患者的预后和NSCLC细胞的恶性表型

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-02 DOI: 10.1111/iep.12436

Na Li, Ling Xu, Ji Zhang, Yongyu Liu

{"title":"High level of FHL2 exacerbates the outcome of non-small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells","authors":"Na Li, Ling Xu, Ji Zhang, Yongyu Liu","doi":"10.1111/iep.12436","DOIUrl":"10.1111/iep.12436","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 Non-small cell lung cancer (NSCLC) is a malignant tumour with high mortality. FHL2 has been identified as a biomarker of lung cancer. This research explored the effects of FHL2 expression on NSCLC. NSCLC-associated data sets were collected from the assistant for clinical bioinformatics and TCGA databases respectively. The association between FHL2 and clinical characteristics, the prognostic significance of FHL2 and the influences of various variables on NSCLC were determined by Pearson's chi-squared test, the Kaplan–Meier curve and the Cox regression model respectively. FHL2 level was altered by cell transfection and was measured by qRT-PCR. Tumour xenograft formation was completed by inoculating sh-FHL2/pcDNA-FHL2 transfected cells into BALB/c nude mice. Protein expression was assessed by western blot. Cell apoptosis, proliferation and epithelial - mesenchymal transition (EMT) characteristics were evaluated employing TUNEL, BrdU+ and microscopic observation respectively. The expression of Ki67 and N-cadherin was assessed by immunohistochemistry. The results showed that FHL2 was highly expressed in NSCLC tissues. Patients with high FHL2 expression experienced lower overall survival probability. FHL2 knockdown promoted apoptosis, but inhibited EMT of A549 and NCI-H460 cells, which was verified by the increased ratios of cleaved caspase 9/caspase 9 and cleaved caspase 3/caspase 3, as well as augmented E-cadherin and reduced N-cadherin. In an in vivo assay FHL2 knockdown decreased tumour volume and weight, repressed EMT, but enhanced apoptosis. FHL2 upregulation showed the opposite effects of FHL2 knockdown. Furthermore, FHL2 upregulation facilitated cell proliferation both in in vitro and in vivo assays. These outcomes indicated that high level of FHL2 facilitated tumorigenesis, as well as the proliferation and EMT of NSCLC cells.\u0000 </section>\u0000 </div>","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 3","pages":"90-101"},"PeriodicalIF":3.0,"publicationDate":"2022-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9556385","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}

引用次数: 3

Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis 柯萨奇病毒B3诱导的心肌炎小鼠模型中一过性心房炎症

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-01 DOI: 10.1111/iep.12438

Ling-Fei Wu, M. D. Fiet, Daan R Raaijmakers, L. Woudstra, A. V. van Rossum, H. Niessen, P. Krijnen

{"title":"Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis","authors":"Ling-Fei Wu, M. D. Fiet, Daan R Raaijmakers, L. Woudstra, A. V. van Rossum, H. Niessen, P. Krijnen","doi":"10.1111/iep.12438","DOIUrl":"https://doi.org/10.1111/iep.12438","url":null,"abstract":"Atrial dysfunction is a relatively common complication of acute myocarditis, although its pathophysiology is unclear. There is limited information on myocarditis‐associated histological changes in the atria and how they develop in time. The aim of this study therefore was to investigate inflammation, fibrosis and viral genome in the atria in time after mild CVB3‐induced viral myocarditis (VM) in mice. C3H mice (n = 68) were infected with 105 PFU of Coxsackievirus B3 (CVB3) and were compared with uninfected mice (n = 10). Atrial tissue was obtained at days 4, 7, 10, 21, 35 or 49 post‐infection. Cellular infiltration of CD45+ lymphocytes, MAC3+ macrophages, Ly6G+ neutrophils and mast cells was quantified by (immuno)histochemical staining. The CVB3 RNA was determined by in situ hybridization, and fibrosis was evaluated by elastic van Gieson (EvG) staining. In the atria of VM mice, the numbers of lymphocytes on days 4 and 7 (p < .05) and days 10 (p < .01); macrophages on days 7 (p < .01) and 10 (p < .05); neutrophils on days 4 (p < .05); and mast cells on days 4 and 7 (p < .05) increased significantly compared with control mice and decreased thereafter to basal levels. No cardiomyocyte death was observed, and the CVB3 genome was detected in only one infected mouse on Day 4 post‐infection. No significant changes in the amount of atrial fibrosis were found between VM and control mice. A temporary increase in inflammation is induced in the atria in the acute phase of CVB3‐induced mild VM, which may facilitate the development of atrial arrhythmia and contractile dysfunction.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"111 1","pages":"149 - 155"},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77596743","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}

引用次数: 3

Transient atrial inflammation in a murine model of Coxsackievirus B3-induced myocarditis 柯萨奇病毒B3诱导的心肌炎小鼠模型中的短暂性心房炎症

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-01 DOI: 10.1111/iep.12438

Linghe Wu, Mitchell D. Fiet, Daan R. Raaijmakers, Linde Woudstra, Albert C. van Rossum, Hans W. M. Niessen, Paul A. J. Krijnen

{"title":"Transient atrial inflammation in a murine model of Coxsackievirus B3-induced myocarditis","authors":"Linghe Wu, Mitchell D. Fiet, Daan R. Raaijmakers, Linde Woudstra, Albert C. van Rossum, Hans W. M. Niessen, Paul A. J. Krijnen","doi":"10.1111/iep.12438","DOIUrl":"https://doi.org/10.1111/iep.12438","url":null,"abstract":"Atrial dysfunction is a relatively common complication of acute myocarditis, although its pathophysiology is unclear. There is limited information on myocarditis-associated histological changes in the atria and how they develop in time. The aim of this study therefore was to investigate inflammation, fibrosis and viral genome in the atria in time after mild CVB3-induced viral myocarditis (VM) in mice. C3H mice (n = 68) were infected with 105 PFU of Coxsackievirus B3 (CVB3) and were compared with uninfected mice (n = 10). Atrial tissue was obtained at days 4, 7, 10, 21, 35 or 49 post-infection. Cellular infiltration of CD45+ lymphocytes, MAC3+ macrophages, Ly6G+ neutrophils and mast cells was quantified by (immuno)histochemical staining. The CVB3 RNA was determined by in situ hybridization, and fibrosis was evaluated by elastic van Gieson (EvG) staining. In the atria of VM mice, the numbers of lymphocytes on days 4 and 7 (p < .05) and days 10 (p < .01); macrophages on days 7 (p < .01) and 10 (p < .05); neutrophils on days 4 (p < .05); and mast cells on days 4 and 7 (p < .05) increased significantly compared with control mice and decreased thereafter to basal levels. No cardiomyocyte death was observed, and the CVB3 genome was detected in only one infected mouse on Day 4 post-infection. No significant changes in the amount of atrial fibrosis were found between VM and control mice. A temporary increase in inflammation is induced in the atria in the acute phase of CVB3-induced mild VM, which may facilitate the development of atrial arrhythmia and contractile dysfunction.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 4","pages":"149-155"},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12438","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71912333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Inflammatory response and immunohistochemical characterization of experimental calcium silicate-based perforation repair material 实验性硅酸钙基穿孔修复材料的炎症反应和免疫组织化学特征

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-04-01 DOI: 10.1111/iep.12439

Hend Okasha, Ashraf M. Abu-Seida, Ahmed A. Hashem, Salma H. El Ashry, Mohamed M. Nagy

{"title":"Inflammatory response and immunohistochemical characterization of experimental calcium silicate-based perforation repair material","authors":"Hend Okasha, Ashraf M. Abu-Seida, Ahmed A. Hashem, Salma H. El Ashry, Mohamed M. Nagy","doi":"10.1111/iep.12439","DOIUrl":"10.1111/iep.12439","url":null,"abstract":"This study compares the immunohistochemical reaction of a new experimental tricalcium silicate perforation repair material to mineral trioxide aggregate (MTA) and Biodentine. A total of 162 mature premolar teeth from 12 dogs were divided into three experimental groups (n = 54 teeth each) according to the evaluation period: 1, 2 and 3 months. Each group was further divided into two equal subgroups (n = 27 teeth each) according to the time of repair: immediate repair and delayed repair. Each subgroup was subdivided according to the material used into three experimental subdivisions (n = 8 teeth each): MTA, Biodentine (Septodont) and experimental material, and two control subdivisions: positive control (n = 2 teeth) and negative control (one tooth). Under general anaesthesia, access cavity was done. Cleaning and shaping were performed using ProTaper universal rotary instruments. The canals were obturated using cold lateral compaction technique with Gutta percha and Adseal sealer. Furcation perforations were created then randomly sealed using the three materials either immediately or after one month (delayed repair). Inflammatory cell count and immunohistochemical analysis of osteopontin-positive area fraction were digitally analysed using the ImageJ software. Delayed furcal perforation repair showed significantly higher inflammatory cell count than immediate repair. No significant difference in inflammatory cell count and immunohistochemical analysis was detected between the three tested materials. The immunohistochemical analysis revealed the highest immunopositive area fraction in the 3-month evaluation period. The experimental tricalcium silicate cement performed similarly to Biodentine and MTA regarding the osteopontin expression during perforation repair, suggesting it is a suitable alternative with favourable handling characters.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 4","pages":"156-163"},"PeriodicalIF":3.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9916164","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}

引用次数: 1

Autoantibodies directed against glutamate decarboxylase interfere with glucose-stimulated insulin secretion in dispersed rat islets 针对谷氨酸脱羧酶的自身抗体干扰分散大鼠胰岛中葡萄糖刺激的胰岛素分泌

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-03-04 DOI: 10.1111/iep.12437

Varun Kamat, Jared R. Radtke, Qingxun Hu, Wang Wang, Ian R. Sweet, Christiane S. Hampe

{"title":"Autoantibodies directed against glutamate decarboxylase interfere with glucose-stimulated insulin secretion in dispersed rat islets","authors":"Varun Kamat, Jared R. Radtke, Qingxun Hu, Wang Wang, Ian R. Sweet, Christiane S. Hampe","doi":"10.1111/iep.12437","DOIUrl":"10.1111/iep.12437","url":null,"abstract":"Islet autoantibodies, including autoantibodies directed against the 65kDa isoform of glutamate decarboxylase (GAD65Ab), are present in the majority of patients with newly diagnosed type 1 diabetes (T1D). Whereas these autoantibodies are historically viewed as an epiphenomenon of the autoimmune response with no significant pathogenic function, we consider in this study the possibility that they impact the major islet function, namely glucose-stimulated insulin secretion. Two human monoclonal GAD65Ab (GAD65 mAb) (b78 and b96.11) were investigated for uptake by live rat beta cells, subcellular localization and their effect on glucose-stimulated insulin secretion. The GAD65 mAbs were internalized by live pancreatic beta cells, where they localized to subcellular structures in an epitope-specific manner. Importantly, GAD65 mAb b78 inhibited, while GAD65 mAb b96.11 enhanced, glucose-stimulated insulin secretion (GSIS). These opposite effects on GSIS rule out non-specific effects of the antibodies and suggest that internalization of the antibody leads to epitope-specific interaction with intracellular machinery regulating insulin granule release. The most likely explanation for the alteration of GSIS by GAD65 Abs is via changes in GABA release due to inhibition or change in GAD65 enzyme activity. This is the first report indicating an active role of GAD65Ab in the pathogenesis of T1D.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 4","pages":"140-148"},"PeriodicalIF":3.0,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9909919","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}

引用次数: 0

Investigation of the effect of metoclopramide on proliferation signal molecules in breast tissue 甲氧氯普胺对乳腺组织增生信号分子影响的研究

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-03-03 DOI: 10.1111/iep.12433

Nurcan Umur, Selda İldan Çalım, Gülce Naz Yazıcı, Seren Gulsen Gurgen

{"title":"Investigation of the effect of metoclopramide on proliferation signal molecules in breast tissue","authors":"Nurcan Umur, Selda İldan Çalım, Gülce Naz Yazıcı, Seren Gulsen Gurgen","doi":"10.1111/iep.12433","DOIUrl":"10.1111/iep.12433","url":null,"abstract":"Metoclopramide (MCP) is a drug that has been widely used in recent years due to its hyperprolactinaemia effect on mothers during breastfeeding. The aim of this study was to investigate the proliferative changes that MCP may cause in the maternal breast tissue. In this study, 18 Wistar albino young–adult breastfeeding mothers with their offspring were divided into three groups: control group, low-dose MCP-applied group and high-dose MCP-applied group. The experiment was carried out during the lactation period and at the end of 21 days. Prolactin, BrdU and Ki-67 breast tissue distributions were evaluated by immunohistochemistry, and tissue levels were evaluated biochemically by the ELISA method. According to ELISA and immunohistochemistry results in breast tissue, there was no significant difference between Ki-67 and BrdU results in all groups. Metoclopramide did not change the expression of proliferation molecules Ki-67 and BrdU in breast tissue. These results suggested that while metoclopramide increases breast proliferation, it does not have the risk of transforming the tissue into a tumour.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 3","pages":"83-89"},"PeriodicalIF":3.0,"publicationDate":"2022-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9547802","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}

引用次数: 0

High-altitude hypoxia-induced rat alveolar cell injury by increasing autophagy 高原缺氧通过增加自噬诱导大鼠肺泡细胞损伤

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2022-03-02 DOI: 10.1111/iep.12434

Zhen Zhao, Bin Hou, Li Tang, Yaping Wang, Yueqing Zhang, Zhanzhuan Ying, Jie Duo

{"title":"High-altitude hypoxia-induced rat alveolar cell injury by increasing autophagy","authors":"Zhen Zhao, Bin Hou, Li Tang, Yaping Wang, Yueqing Zhang, Zhanzhuan Ying, Jie Duo","doi":"10.1111/iep.12434","DOIUrl":"10.1111/iep.12434","url":null,"abstract":"Autophagy has been implicated in the pathogenesis of various lung diseases. This study aimed to investigate the role of autophagy in lung injury induced by high-altitude hypoxia. Wistar rats were randomized into four groups for exposure to normal altitude or high altitude for 1, 7, 14 and 21 days with no treatment or with the treatment of 1 mg/kg rapamycin or 2 mg/kg 3-methyladenine (3-MA) for consecutive 21 days respectively. In control rats, the alveolar structure was intact with regularly arranged cells. However, inflammatory cell infiltration and shrunk alveoli were observed in rats exposed to hypoxia. Rapamycin treatment led to many shrunken alveoli with a large number of red blood cells in them. In contrast, 3-MA treatment led to almost intact alveoli or only a few shrunken alveoli. Compared to the control group exposure to high-altitude hypoxia for longer periods resulted in the aggravation of the lung injury, the formation of autophagosomes with a double-membrane structure and increased levels of Beclin-1 and LC3-II in alveolar tissues. Rapamycin treatment resulted in significant increase in Beclin-1 and LC3-II levels and further aggravation of alveolar tissue damage, while 3-MA treatment led to opposite effects. In conclusion, exposure to high-altitude hypoxia can induce autophagy of alveolar cells, which may be an important mechanism of high-altitude hypoxia-induced lung injury. The inhibition of autophagy may be a promising therapy strategy for high-altitude hypoxia-induced lung injury.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"103 4","pages":"132-139"},"PeriodicalIF":3.0,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9913225","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}

引用次数: 0