Folia histochemica et cytobiologica最新文献

{"title":"Decreased immunoreactivity of von Willebrand factor may reflect persistent nature of the endothelial dysfunction in non-ischemic heart failure.","authors":"Edyta Reichman-Warmusz,&nbsp;Marlena Brzozowa-Zasada,&nbsp;Celina Wojciechowska,&nbsp;Damian Dudek,&nbsp;Oliwia Warmusz,&nbsp;Romuald Wojnicz","doi":"10.5603/FHC.a2021.0012","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0012","url":null,"abstract":"<p><strong>Introduction: </strong>Endothelial dysfunction is a critical part of heart failure (HF) pathophysiology. It is not clear, however, whether it is present at the similar level in the early and late HF stages.</p><p><strong>Material and methods: </strong>von Willebrand factor (vWF) and its mRNA levels in biopsies of non-ischemic patients with HF secondary to dilated cardiomyopathy were studied. Consecutive patients with HF were divided into two groups: group A with disease duration ≤ 12 months (n = 59) and group B with disease duration > 12 months (n = 68). The immunoreactivity of the vWF was compared with autopsy sections of 19 control cases. Tissue vWF gene expression was analyzed at the mRNA level by RT-PCR.</p><p><strong>Results: </strong>In the group A, there was lower vWF immunoreactivity in the coronary microvessels compared to the group B [1.5 (1.0-2.0) vs. 2.0 (1.5-2.4), P = 0.001]. In the control group, only weak vWF expression was observed. Protein expression was not accompanied by vWF mRNA whose levels were significantly higher in the Group A as compared to the Group B [14671 (4932-51561) vs. 3643 (185.3-9030.8), P = 0.005]. Protein vWF expression was inversely associated with its mRNA levels (r = -0.34, P = 0.04).</p><p><strong>Conclusions: </strong>High myocardial protein expression of vWF in patients with long-lasting HF symptoms may highlight the persistent nature of endothelial dysfunction in such a cohort of patients.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 2","pages":"108-113"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38912213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus polysaccharide protects formaldehyde-induced toxicity by promoting NER pathway in bone marrow mesenchymal stem cells.","authors":"Yali She,&nbsp;Xiaowen Zhao,&nbsp;Pingfan Wu,&nbsp;Ling Xue,&nbsp;Zhe Liu,&nbsp;Meng Zhu,&nbsp;Jie Yang,&nbsp;Yaling Li","doi":"10.5603/FHC.a2021.0013","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0013","url":null,"abstract":"<p><strong>Introduction: </strong>In our previous study, it has been confirmed that formaldehyde (FA) not only inhibits the proliferative activity, but also causes DNA-protein crosslinks (DPCs) formation in bone marrow mesenchymal stem cells (BMSCs). The purpose of this study was to detect the protective effect of astragalus polysaccharide (APS) against the cytotoxicity and genotoxicity of BMSCs exposed to FA, and to explore potential molecular mechanisms of APS activity.</p><p><strong>Material and methods: </strong>Human BMSCs were cultured in vitro and randomly divided into control cells (Ctrl group), FA-treated cells (FA group, 120 μmol/L), and cells incubated with FA and increasing concentrations (40, 100, or 400 μg/mL) of APS (FA + APS groups). Cytotoxicity was measured by MTT assay. DNA strand breakage, DNA-protein crosslinks (DPCs), and micronucleus formation were respectively detected by comet assay, KCl-SDS precipitation assay, and micronucleus assay. The mRNA and protein expression level of xeroderma pigmentosum group A (XPA), xeroderma pigmentosum group C (XPC), excision repair cross-complementation group 1 (ERCC1), replication protein A1 (RPA1), and replication protein A2 (RPA2) were all detected by qRT-PCR and Western Blot.</p><p><strong>Results: </strong>Compared with the FA group, the cytotoxicity, DNA strand breakage, DPCs, and micronucleus levels were decreased significantly in FA + APS groups (P < 0.01). Meanwhile, the mRNA and protein expression of XPA, XPC, ERCC1, RPA1, and RPA2 were up regulated significantly in the FA + APS groups (P < 0.05) with the most prominent effect of the 100 μg/mL APS.</p><p><strong>Conclusions: </strong>Our results suggest that APS can protect the cytotoxicity and genotoxicity of human BMSCs induced by FA. The mechanism may be associated with up-regulated expression of XPA, XPC, ERCC1, RPA1, and RPA2 in the nucleotide excision repair (NER) pathway which promotes DNA damage repair.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 2","pages":"124-133"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38997892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-term fenofibrate treatment improves ultrastructure of hepatocytes of old rats.","authors":"Adrian Zubrzycki,&nbsp;Agata Wronska,&nbsp;Agata Zauszkiewicz-Pawlak,&nbsp;Zbigniew Kmiec","doi":"10.5603/FHC.a2021.0018","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0018","url":null,"abstract":"<p><strong>Introduction: </strong>Fenofibrate (FN) is a hypolipemic drug used for the treatment of mixed dyslipidemia. Since in our previous study FN administration to young and old rats adversely affected the serum activity of liver marker enzymes, we decided to examine the effects of FN on liver ultrastructure of young and old animals.</p><p><strong>Material and methods: </strong>Young and old rats were fed standard rodent chow supplemented with 0.1% FN for 30 days. Liver samples obtained from animals under full anesthesia were processed by routine methods to obtain ultrathin and histological sections for the examination by light microscopy (LM) and transmission electron microscopy (TEM). Furthermore, liver lysates were analyzed by Western blotting for the expression of the autophagy-related proteins LC3A/B and beclin 1.</p><p><strong>Results: </strong>The ultrastructure of hepatocytes in both age groups was well-preserved, with the presence of abundant mitochondria, numerous peroxisomes and lysosomes, glycogen stored in the form of rosettes, and occasionally autolysosomes. However, hepatocytes of old control rats contained less mitochondria and peroxisomes, and more lipid droplets than cells of young animals. The effects of FN on liver ultrastructure were age-depended. FN increased the relative number of mitochondria and peroxisomes in the hepatocytes of old, and did not affect their number in young rats. Moreover, FN decreased and increased the relative number of lipid droplets in the hepatocytes of old and young rats, respectively. At the LM level, Oil Red O staining revealed smaller and larger lipid droplets within hepatocytes and non-parenchymal liver cells. In the livers of young and old rats lipid droplets were distributed mainly in the periportal zones of hepatic lobules. Morphometric analysis confirmed that livers of control old rats contained more lipid-stainable areas than those of young ones; however, no effect of FN was observed either in young or old rats. Despite larger size of autolysosomes and autophagic vacuoles in hepatocytes of old rats, the expression of autophagy-related proteins did not differ in the livers of control and fenofibrate-treated young and old animals.</p><p><strong>Conclusions: </strong>The results of our study suggest that fenofibrate, apart from its hypolipemic action, may have beneficial effect on the energy metabolism in the liver of old individuals by increasing the number of mitochondria and peroxisomes in hepatocytes.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 3","pages":"167-177"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39411177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LYAR promotes the proliferation of non-small cell lung cancer and is associated with poor prognosis.","authors":"Xiao-Ning Lu,&nbsp;Guan-Jun Ju,&nbsp;Yu-Xin Wang,&nbsp;Yong-Liang Wang,&nbsp;Kun Wang,&nbsp;Jian-Le Chen,&nbsp;Wei Cai,&nbsp;Qi-Wei Zang","doi":"10.5603/FHC.a2021.0030","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0030","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of the study was to investigate the clinical significance of Ly-1 antibody reactive clone (LYAR) in non-small-cell lung cancer (NSCLC).</p><p><strong>Material and methods: </strong>The expressions of LYAR at the protein level in representative paired NSCLC tumor tissues and adjacent non-tumor tissues were measured by Western blot and immunohistochemistry. Kaplan-Meier method was used to calculate the survival curve of patients with NSCLC. Cell Counting Kit-8 assay and flow cytometry were used to estimate the cell proliferation and cell cycle, respectively. Terminal-deoxynucleotidyl-transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was performed to detect cell apoptosis.</p><p><strong>Results: </strong>LYAR was dramatically overexpressed in NSCLC tissues which were closely related to the survival of patients with NSCLC. In clinical studies, the expression of LYAR was related to the clinical stage, histological differentiation, and Ki-67 expression. A positive correlation was found between LYAR and Ki-67 expression by Spearman's correlation test. After serum starvation for 72 h, serum re-addition significantly increased the expression of LYAR, PCNA, and Cyclin A and promoted the cell cycle progression. LYAR knockdown inhibited the proliferation and induced the G0/G1 cell cycle arrest and apoptosis of A549 cells.</p><p><strong>Conclusions: </strong>The present study revealed the clinical significance of LYAR in NSCLC. LYAR might serve as a tumor promoter in NSCLC progression by promoting the proliferation and inhibiting the apoptosis of NSCLC cells. Inhibiting the expression of LYAR was considered as a potential novel therapeutic strategy for NSCLC.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 4","pages":"282-290"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39711307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-140-5p inhibits the proliferation, migration and invasion of vascular smooth muscle cells by suppressing the expression of NCKAP1.","authors":"Qing Ma,&nbsp;Jiancheng Liu,&nbsp;Chunbo Li,&nbsp;Dong Wang","doi":"10.5603/FHC.a2021.0003","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0003","url":null,"abstract":"<p><strong>Introduction: </strong>The occurrence of aortic dissection is related to the proliferation and metastasis of vascular smooth muscle cells. In our present study, we found that the expression of miR-140-5p was inhibited in the wall of abdominal aorta of aortic dissection patients. However, the mechanism of miR-140-5p in the development of aortic dissection is unclear.</p><p><strong>Material and methods: </strong>We detected the expression of miR-140-5p and NCK Associated Protein 1 (NCKAP1) in blood vessel of aortic dissection patients and normal people by PCR. Next, we established the miR-140-5p overexpression and miR-140-5p inhibition vascular smooth muscle cells (CRL-1999 cells). The BrdU assays, wound healing assays and transwell assays were performed to detect the proliferation and invasion ability of these cells. Finally, luciferase reporter assay was performed to detect the relationship between miR-140-5p and NCKAP1.</p><p><strong>Results: </strong>The expression of miR-140-5p was suppressed in blood vessel of aortic dissection patients, and the levels of NCKAP1 in those tissues were upregulated. Overexpression of miR-140-5p inhibited the proliferation, migration and invasion of vascular smooth muscle cells. miR-140-5p targeted and suppressed the expression of NCKAP1.</p><p><strong>Conclusions: </strong>miR-140-5p repressed the proliferation, migration and invasion of vascular smooth muscle cells by targeting and inhibiting the expression of NCKAP1. Furthermore, the results of our study suggest new strategies and targets for the clinical treatment of arterial dissection.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 1","pages":"22-29"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25347931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Actinidia chinensis Planch. root extract inhibits the proliferation, migration and invasion of breast cancer cells via the AKT/GSK-3β signaling pathway.","authors":"Chunchun Gan,&nbsp;Zhan Jin,&nbsp;Xiaopeng Wei,&nbsp;Meina Jin","doi":"10.5603/FHC.a2021.0023","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0023","url":null,"abstract":"<p><strong>Introduction: </strong>Actinidia chinensis Planch. root extract (acRoots), known as a traditional Chinese medicine (TCM), has shown antitumor efficacy in various types of human cancers. However, its role and underlying mechanisms in breast cancer (BCa) have not been elucidated.</p><p><strong>Material and methods: </strong>In the present study, the effects of acRoots on cell viability, apoptosis, migration and invasion were analyzed by MTT assay, colony formation, flow cytometry, wound healing and Transwell assay in MDA-MB-231 and MDA-MB-453 breast cancer cell lines. The expression levels of relevant proteins were determined by Western blot assay.</p><p><strong>Results: </strong>The results revealed that acRoots inhibited proliferation, migration, and invasion and promoted apoptosis of BCa cells. Moreover, acRoots decreased the expression of cyclin D1, survivin, Bcl-2, N-cadherin, and Snail and increased the expression of Bax and E-cadherin in MDA-MB-231 and MDA-MB-453 cells. AcRoots inhibited the AKT/GSK-3b pathway by decreasing the levels of phosphorylated AKT, phosphorylated GSK-3b and b-catenin.</p><p><strong>Conclusions: </strong>The described effects of acRoots on the cultured BCa cells suggest that they may be mediated by the inhibition of the AKT/GSK-3b signaling pathway. Thus, further studies are warranted to test the possibility that AcRoots may be used as a promising anticancer agent for breast cancer treatment.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 4","pages":"226-235"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39682787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genistein exerts a cell-protective effect via Nrf2/HO-1/ /PI3K signaling in Ab25-35-induced Alzheimer's disease models in vitro.","authors":"Shanqing Yi,&nbsp;Shuangxi Chen,&nbsp;Jian Xiang,&nbsp;Jian Tan,&nbsp;Kailiang Huang,&nbsp;Hao Zhang,&nbsp;Yilin Wang,&nbsp;Heng Wu","doi":"10.5603/FHC.a2021.0006","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0006","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD), a very common neurodegenerative disorder, is mainly characterized by the deposition of b-amyloid protein (Ab) and extensive neuronal cell death. Currently, there are no satisfactory therapeutic approaches for AD. Although neuroprotective effects of genistein against Ab-induced toxicity have been reported, the underlying molecular mechanisms remain unclear. Furthermore, the PI3K/Akt/Nrf2 signaling pathway is associated with AD. The aim of the study was to investigate whether genistein can modulate Nrf2/HO-1/PI3K signaling to treat AD.</p><p><strong>Materials and methods: </strong>Cell viability assay, the measurement of heme oxygenase-1 (HO-1) expression by reverse transcription-polymerase chain reaction (RT-qPCR), and western blot were performed on the SH-SY5Y cells induced by Ab25-35 in response to the treatment with genistein. Moreover, PI3K p85 phosphorylation was measured.</p><p><strong>Results: </strong>Genistein enhanced the HO-1expression at both the mRNA and protein levels, as well as the PI3K p85 phosphorylation level. In addition, genistein increased the survival of SH-SY5Y cells treated with Ab25-35via HO-1 signaling. However, following transfection with Nrf2 small interfering RNA (siRNA) and treatment with LY294002, an inhibitor of PI3K p85, genistein could not upregulate HO-1 to exert neuroprotective effects on SH-SY5Y cells treated with Ab25-35.</p><p><strong>Conclusions: </strong>These results suggest that genistein exerts a neuroprotective effect on SH-SY5Y cells in vitro via Nrf2/ HO-1/PI3K signaling, providing a foundation for the application of genistein in the treatment of neurodegenerative diseases related to Nrf2/HO-1/PI3K signaling.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 1","pages":"49-56"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25384257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current status and development trend of miRNAs in osteoporosis-related research: A bibliometric analysis.","authors":"Li Yun,&nbsp;Lining Wang,&nbsp;Yalan Pan,&nbsp;Mengmin Liu,&nbsp;Qiuge Han,&nbsp;Jie Sun,&nbsp;Guanglu Yang,&nbsp;Jirimutu Xiao,&nbsp;Yang Guo,&nbsp;Yong Ma","doi":"10.5603/FHC.a2021.0024","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0024","url":null,"abstract":"<p><strong>Introduction: </strong>The occurrence of osteoporosis (OP) has drawn considerable attention from scholars around the world due to the significant impacts thereof on the social economy and the quality of human life. OP research has been rapidly expanding since the inclusion of microRNAs (miRNAs) as critical regulators of gene-expression. However, despite the ability to evaluate miRNA gene therapy in OP being enhanced, there has been a scarcity of updated citation analyses that reflect such developments. In the present study, through bibliometric analysis, the global research activity and trends in regard to the relationship between OP and miRNAs were reviewed.</p><p><strong>Methods: </strong>Publications related to miRNA and OP from 2000 to 2021 were retrieved via Web of Science (WoS). The data included publication years, countries, journals, institutions, authors and keywords, and were sorted and summarized by bibliometrics, before being visually analyzed through VOS Viewer.</p><p><strong>Results: </strong>In the past five years, 599 articles have been published, with said studies accounting for 79.11% of all relevant documents, indicating the increased interest in the present research topic. The country with the highest contribution rate was China, and the publication rate of Journal of Bone and Mineral Research was the highest, followed by Bone. The institutions with the highest contribution rate were Nanjing Medical University. The most frequently occurring keywords were clustered into five groups. The research area of the first group described that circulating miRNA would be a potential biomarker for postmenopausal osteoporosis (PMOP). The remaining four groups involved the influences of miRNAs and exosomes on the osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs), and the interactions of lncRNA and miRNA with OP.</p><p><strong>Conclusions: </strong>The results of the present study will expand the research on miRNAs and OP. The research direction with the highest frequency was the miRNAs acting on osteoblasts and osteoclasts. The influence of miRNAs carried by exosomes on the differentiation of MSCs might become an effective method for OP cell-free treatment.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 4","pages":"203-211"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39935297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenovirus-mediated RNA interference against herpes simplex virus infection in vitro.","authors":"Lin Chen,&nbsp;Zhi-Qiang Pan,&nbsp;Chang-Bin Zhai","doi":"10.5603/FHC.a2021.0031","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0031","url":null,"abstract":"<p><strong>Introduction: </strong>Herpetic keratitis caused by the herpes simplex virus (HSV) is the most common form of ocular herpes that causes corneal blindness. Although treatments for herpes keratitis have improved in recent years. there is still considerable room for new treatments against viral infection that shows great promise. The aim of the study was to evaluate the effect of RNA interference on HSV Type 1 (HSV1) infection in vitro, first prophylactically then therapeutically.</p><p><strong>Material and methods: </strong>The highly conserved glycoproteins D (gD) and E (gE) were chosen as targets for this study. Different small interfering RNA (siRNA) duplexes that target gD and gE were designed and chemically synthesized. The recombinant adenovirus type 5 was developed and used as the vehicle with which we delivered the siRNA into the Vero cells infected with the HSV1 KOS strain. Evaluation of the efficacy of siRNA-mediated inhibition was performed either before virus inoculation (prophylactically) or after virus inoculation at the first appearance of lesions (therapeutically). The expression of messenger RNA encoding gD and gE was detected using a real-time polymerase chain reaction (qPCR). We analyzed HSV replication in Vero cells, cytotoxicity of HSV, and cell viability.</p><p><strong>Results: </strong>When used prophylactically, the siRNA-targeting gD and gE created a more marked decrease in viral titer than when used therapeutically. The transfection of cells with recombinant adenovirus containing the siRNA expression cassette was associated with very low cytotoxicity.</p><p><strong>Conclusions: </strong>Adenovirus-mediated siRNA-targeting gD and gE genes effectively inhibit the replication of the HSV in Vero cells. In addition, these findings indicate that the prophylactic use of siRNA is far more effective at inhibiting HSV replication than the therapeutic use.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 4","pages":"302-310"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39723475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of e-cigarette flavoring agents on the neural retina of chick embryo: histological and gene expression study.","authors":"Malak Alshareef,&nbsp;Aziza Alrafiah,&nbsp;Sara Abed,&nbsp;Fatemah Basingab,&nbsp;Aisha Alrofaidi","doi":"10.5603/FHC.a2021.0028","DOIUrl":"https://doi.org/10.5603/FHC.a2021.0028","url":null,"abstract":"<p><strong>Background: </strong>An electronic cigarette (e-cigarette) is initially marketed as an assistant product to quit smoking or limit its use. However, recent studies suggest the opposite, describing it as a product that lacks adequate quality and user safety. The present study aimed to investigate the effect of e-cigarette flavoring agent (cinnamon flavor) on the neural retina development of chick embryos and apoptosis induction after the early and late apoptosis stages by quantitative detection of gene expression CASP-3 at both embryonic days E9 and E17.</p><p><strong>Methods: </strong>Fertilized chicken eggs were divided into two groups: control and treatment, and each group included two embryonic days; E9 and E17. For each treatment stage, two dosages of the treatment were applied, 2% and 5%. The neural retinas were dissected from the sclera and retinal pigment epithelium for subsequent RNA extraction and histological examination.</p><p><strong>Results: </strong>This study indicated that aerosol of the subtle cinnamon flavor e-liquid causes downregulated expression of CASP3 in neural retina development. In addition, the hematoxylin and eosin (H&E)-stained sections showed multiple structural changes in the retinal layers and evidence of apoptotic cell death.</p><p><strong>Conclusion: </strong>Cell death was visible and abundant in E9, and E17 concludes that flavor vapor condensate treatment caused neuronal cell death. CASP-3 was downregulated, which indicates that cell death occurred independently of CASP-3.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"59 4","pages":"245-258"},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39807239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}