Molecular & Cellular Toxicology最新文献_第6页

Evaluation of the antinociceptive effect and standardization of Platycladus orientalis (L.) Franco extract 东方桔梗（L. ）弗朗科提取物的抗痛觉作用和标准化评估

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2024-01-26 DOI: 10.1007/s13273-023-00413-7

{"title":"Evaluation of the antinociceptive effect and standardization of Platycladus orientalis (L.) Franco extract","authors":"","doi":"10.1007/s13273-023-00413-7","DOIUrl":"https://doi.org/10.1007/s13273-023-00413-7","url":null,"abstract":"<h3>Abstract</h3> <span> <h3>Background</h3> <p><em>Platycladus orientalis</em> (L.) Franco (PO) has been used in Oriental medicine to treat rheumatism and diarrhea; however, its antinociceptive effects remain unclear.</p> </span> <span> <h3>Objective</h3> <p>This study aimed to reveal the antinociceptive effect of the PO extract and standardize this extract in RAW 264.7 cells and mice with monosodium uric acid (MSU)-induced pain.</p> </span> <span> <h3>Results</h3> <p>PO extracts were prepared using different ethanol (EtOH) concentrations (0–100%). Thereafter, groups were determined based on the results of the MSU-induced pain model in mice and nitric oxide (NO) assay using lipopolysaccharide (LPS)-induced RAW 264.7 cells. As the methylene chloride (CH<sub>2</sub>Cl<sub>2</sub>) and ethyl acetate (EtOAc) layers exhibited increasing effects with time, these layers were selected to isolate the major components. The PO extract was standardized using a highly efficient HPLC method, and its antinociceptive effects in a mouse model of MSU-induced gout pain were determined using the von Frey test. The PO extract was found to exhibit antinociceptive effects. Moreover, sample standardization was successfully achieved based on the validation of these compounds.</p> </span> <span> <h3>Conclusion</h3> <p>The PO extract exhibited potent dose- and time-dependent antinociceptive effects in an animal model of gout pain; these effects might be mediated by the major compounds of this extract. Collectively, these results suggest that PO can be used as a herbal drug to treat gout-related pain.</p> </span>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"3 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139587884","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

Bone marrow mesenchymal stem cell transplantation protects rats from myocardial infarction by regulating TXNIP/NLRP3 pathway-mediated inflammation and fibrosis 骨髓间充质干细胞移植通过调节 TXNIP/NLRP3 通路介导的炎症和纤维化，保护大鼠免受心肌梗死之苦

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2024-01-25 DOI: 10.1007/s13273-023-00422-6

JianNan Bai, Cong Wang, HongQiang Yu, QingChao Wang, JinFeng Zhang, DanDan Shao, ZhiQiang Yu, Bo Meng, You Li

{"title":"Bone marrow mesenchymal stem cell transplantation protects rats from myocardial infarction by regulating TXNIP/NLRP3 pathway-mediated inflammation and fibrosis","authors":"JianNan Bai, Cong Wang, HongQiang Yu, QingChao Wang, JinFeng Zhang, DanDan Shao, ZhiQiang Yu, Bo Meng, You Li","doi":"10.1007/s13273-023-00422-6","DOIUrl":"https://doi.org/10.1007/s13273-023-00422-6","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Bone marrow mesenchymal stem cells (BMSCs) may be a promising target in the treatment of myocardial infarction (MI). However, the underlying molecular mechanisms of BMSC therapy remain unclear.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This study sought to evaluate the efficacy of direct intramyocardial transplantation of BMSCs in a mouse model of MI.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Mouse BMSCs were transfected with small interfering RNA or overexpression plasmid targeting TXNIP. The viability, proliferation, and apoptosis of BMSCs after hypoxia treatment were detected by MTT method, EdU analysis, and flow cytometry, respectively. A mouse model of MI was constructed, after which BSMCs were injected intramyocardially immediately. Cardiac ultrasound, HE staining, TUNEL staining and ELISA, IHC analysis, and Western blot were adopted to evaluate the effects of BSMC therapy on cardiac function, myocardial inflammation, and fibrosis in mice.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>In vitro experiments reported that ablating TXNIP increased viability and inhibited apoptosis of hypoxia-treated BMSCs while overexpressing TXNIP did the opposite. In vivo results stated that BSMCs improved cardiac function, myocardial inflammation, and fibrosis after MI, which was further improved by silencing TXNIP but reversed by overexpressing TXNIP. Meanwhile, in vivo cell tracking experiments showed that the retained BMSCs in the myocardium decreased after transplantation, and TXNIP depletion promoted the survival of BMSCs in MI mice, whereas TXNIP overexpression did the opposite.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>In conclusion, BMSC transplantation improves cardiac function, myocardial inflammation, and fibrosis after MI by regulating the TXNIP/NLRP3 pathway.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"89 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139588001","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

Olaparib synergically exacerbates the radiation-induced intestinal apoptosis in mice 奥拉帕利协同加剧辐射诱导的小鼠肠道凋亡

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2024-01-20 DOI: 10.1007/s13273-023-00421-7

{"title":"Olaparib synergically exacerbates the radiation-induced intestinal apoptosis in mice","authors":"","doi":"10.1007/s13273-023-00421-7","DOIUrl":"https://doi.org/10.1007/s13273-023-00421-7","url":null,"abstract":"<h3>Abstract</h3> <span> <h3>Background</h3> <p>Olaparib, a poly [ADP-ribose] polymerase (PARP) inhibitor, is used in cancer treatment and in other diseases and achieves local cancer control in combination with radiotherapy.</p> </span> <span> <h3>Objectives</h3> <p>We investigated the effects of olaparib on irradiation-induced intestinal damage using both in vitro and in vivo model systems. In particular, we evaluated how olaparib affects irradiation-induced cytotoxicity in intestinal epithelial (IEC-6) cell line and intestinal damage in mice subjected to abdominal radiation.</p> </span> <span> <h3>Results</h3> <p>Using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays to evaluate radiation-induced cytotoxicity and the loss of cell viability, we found that olaparib pretreatment significantly exacerbated radiation-induced effects. Olaparib therapy increased protein expression related to radiation-induced DNA damage. Administering per oral olaparib (100 mg/kg) to adult mice from − 2 to 0 days before radiation exposure (10 or 15 Gy) significantly accelerated intestinal damage. Measurements of the small intestinal villi length and number of crypts were collected through histological investigations. The irradiation group showed shorter crypt survival and jejunal villi height than the sham-irradiated group. In addition, through the TUNEL assay, we were able to confirm an increased apoptotic rate of enterocytes in the group pretreated with olaparib before 10 Gy of irradiation compared with the dose-matched irradiation group.</p> </span> <span> <h3>Conclusion</h3> <p>In radiation-exposed mice, olaparib therapy significantly reduced indicators such as the length of the small intestinal villi and number of crypts. Administering olaparib before radiation aggravated the radiation-induced damage to the jejunum and exacerbated intestinal apoptosis. Olaparib in combination with radiotherapy should be used cautiously in patients with cancer.</p> </span>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"30 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510219","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

Genotoxicity evaluation of collagen peptide derived from skate (Raja kenojei) skin: In vitro and in vivo studies 鳐鱼（Raja kenojei）皮肤胶原蛋白肽的遗传毒性评估：体外和体内研究

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2024-01-19 DOI: 10.1007/s13273-023-00423-5

Heung-Sik Seo, Ji-Soo Kim, Myeong-Kyu Park, Nak-Won Seong, Geun-Hee Kang, Sang-Ho Kim, Joong-Sun Kim, Sung-Ho Kim, Jong-Choon Kim, Changjong Moon

{"title":"Genotoxicity evaluation of collagen peptide derived from skate (Raja kenojei) skin: In vitro and in vivo studies","authors":"Heung-Sik Seo, Ji-Soo Kim, Myeong-Kyu Park, Nak-Won Seong, Geun-Hee Kang, Sang-Ho Kim, Joong-Sun Kim, Sung-Ho Kim, Jong-Choon Kim, Changjong Moon","doi":"10.1007/s13273-023-00423-5","DOIUrl":"https://doi.org/10.1007/s13273-023-00423-5","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>The medicinal properties and benefits of collagen peptides (CPs) are widely recognized and utilized. However, the potential genotoxicity of CPs remains elusive.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>The objective of this study was to assess the potential genotoxicity of CP derived from skate (<i>Raja kenojei</i>) skin (CPSS). To achieve this, we conducted a comprehensive study using three standard battery systems in accordance with the test guidelines provided by the Organisation for Economic Cooperation and Development and the Korean Ministry of Food and Drug Safety, as well as the principles of Good Laboratory Practice.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>We performed a bacterial reverse mutation (Ames) test using the pre-incubation method, with or without a metabolic activation system (S9 mixture). The Ames test, conducted on <i>Salmonella typhimurium</i> strains TA98, TA100, TA1535, and TA1537, as well as <i>Escherichia coli</i> strain WP2<i>uvr</i>A, demonstrated that CPSS did not cause gene mutations in any of the tested strains, regardless of the dose level. In addition, we performed an in vitro chromosome aberration test using cultured Chinese hamster lung fibroblast cells, with and without the S9 mixture, and an in vivo mouse bone marrow micronucleus test on specific pathogen-free male ICR mice. Both the in vitro chromosomal aberration test and the in vivo micronucleus test revealed no chromosomal aberrations resulting from CPSS treatment.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Our findings demonstrate that CPSS does not exhibit mutagenic or clastogenic activity in either in vitro or in vivo test systems, supporting its potential as a safe material for medical use.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"7 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139497867","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

Phenotypic and functional alterations of bone marrow MSCs exposed to multiple myeloma cells 暴露于多发性骨髓瘤细胞的骨髓间充质干细胞的表型和功能改变

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-12-16 DOI: 10.1007/s13273-023-00415-5

{"title":"Phenotypic and functional alterations of bone marrow MSCs exposed to multiple myeloma cells","authors":"","doi":"10.1007/s13273-023-00415-5","DOIUrl":"https://doi.org/10.1007/s13273-023-00415-5","url":null,"abstract":"<h3>Abstract</h3> <span> <h3>Backgrounds</h3> <p>The direct and indirect interactions between multiple myeloma (MM) cells and bone marrow mesenchymal stromal cells (MSCs) play crucial roles in the formation of the bone marrow environment, disease progression, and drug resistance development. However, it remains unclear how MM cells and MSCs individually influence each other to induce these phenomena.</p> </span> <span> <h3>Objective</h3> <p>In this study, we focused on observing changes in MSCs induced by MM cells. Changes in MSCs due to exposure to MM cells were observed by assessing cell proliferation, apoptosis, cell cycle, and morphology. Furthermore, the unique abilities of MSCs were confirmed through differentiation potential and MSC marker expression, along with the demonstration of senescence. Gene profiling was performed to elucidate the mechanisms underlying these changes.</p> </span> <span> <h3>Results</h3> <p>Co-culturing MM cells with MSCs did not alter the morphology or proliferation of MSCs but increased apoptosis. As apoptosis increased, damaged deoxyribonucleic acid (DNA) was repaired, leading to the activation of the cell cycle with an increase in the S phase, resulting in no significant changes in cell proliferation and morphology. Osteogenesis and adipogenesis generally decreased by co-culturing with MM cells, and senescence increased. Significant differences were observed in the expression of MSC marker genes. Gene profiling revealed changes in gene expression following osteogenic differentiation.</p> </span> <span> <h3>Conclusion</h3> <p>Based on these results, MSCs exposed to MM cells exhibited an increase in the S phase of the cell cycle, leading to the recovery of cells undergoing apoptosis. Osteogenesis and adipogenesis decreased, whereas senescence increased, suggesting that these changes were attributed to the overall MSC characteristics and genetic mechanisms.</p> </span>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"30 1 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138685097","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

Maslinic acid induces apoptosis in thyroid cancer cells via endoplasmic reticulum stress 马钱子酸通过内质网应激诱导甲状腺癌细胞凋亡

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-12-12 DOI: 10.1007/s13273-023-00406-6

Jing Zhu, Pinghui Tu, Yu Yang, Dandan Zhang, Fengling Chen

{"title":"Maslinic acid induces apoptosis in thyroid cancer cells via endoplasmic reticulum stress","authors":"Jing Zhu, Pinghui Tu, Yu Yang, Dandan Zhang, Fengling Chen","doi":"10.1007/s13273-023-00406-6","DOIUrl":"https://doi.org/10.1007/s13273-023-00406-6","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Thyroid cancer is one of the most common malignant tumors of the endocrine system. Studies have demonstrated that maslinic acid (MA) has a wide range of antitumor activities via multiple cellular pathways. However, the role of MA in thyroid cancer remains poorly investigated.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>To investigate the effects and underlying mechanisms of MA on thyroid cancer cells.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>MA inhibited cell viability and increased apoptosis in TPC1 and Cal62 cells. MA promoted apoptosis in TPC1 and Cal62 cells in a dose-dependent manner evidenced by flow cytometry and Western blotting. In addition, treatment with MA increased the expression of endoplasmic reticulum (ER) stress markers, such as Binding-immunoglobulin protein (BIP) and C/EBP homologous protein 10 (CHOP), in thyroid cancer cells. In cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, MA-induced apoptosis was partially reversed. Finally, treatment with MA inhibited thyroid cancer growth in a TPC1 cell xenograft model.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Results indicated that MA promoted apoptosis in thyroid cancer cells via ER stress. These findings may provide new insights into novel therapeutic strategies for thyroid cancer.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"73 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138573965","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

The mechanism of 5-aminolevulinic acid-photodynamic therapy pretreatment repressing keloid fibroblast proliferation and invasion by mediating forkhead box protein O6 (FoxO6) antioxidant stress 5-氨基乙酰丙酸-光动力疗法预处理通过介导叉头盒蛋白O6（FoxO6）抗氧化应激抑制瘢痕疙瘩成纤维细胞增殖和侵袭的机制

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-12-07 DOI: 10.1007/s13273-023-00417-3

Qiong Wang, Weihui Zeng, Shuang Wang, Songmei Geng, Chen Tu

{"title":"The mechanism of 5-aminolevulinic acid-photodynamic therapy pretreatment repressing keloid fibroblast proliferation and invasion by mediating forkhead box protein O6 (FoxO6) antioxidant stress","authors":"Qiong Wang, Weihui Zeng, Shuang Wang, Songmei Geng, Chen Tu","doi":"10.1007/s13273-023-00417-3","DOIUrl":"https://doi.org/10.1007/s13273-023-00417-3","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Objective</h3><p>Keloid is a kind of disfiguring pathological scarring specific to human skin. For various cutaneous and internal tumours, 5-aminolevulinic acid-photodynamic therapy (5-ALA-PDT) is a curative choice, and we explored its mechanism on keloid fibroblast (KFB) proliferation and invasion via regulating forkhead box protein O6 (FoxO6) antioxidant stress.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Human keloid fibroblasts (HKFs) were cultured in vitro, treated with 5-ALA-PDT and simultaneously transfected with overexpression plasmid (oe-FoxO6). HKF proliferation, invasion, apoptosis and cell cycle were assessed by CCK-8/Transwell/TUNEL/flow cytometry assays. The protein levels of Bax, Bcl-2, FoxO6, Cyclin D1, Cyclin A1 and Cyclin B1 were determined by Western blot. SOD and CAT activities, and MDA and ROS levels were examined using the kits.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Pretreatment of 5-ALA-PDT prominently inhibited the proliferation of HKFs, up-regulated Bax level, down-regulated Bcl-2 level, promoted HKF apoptosis, and notably inhibited HKF invasion. 5-ALA-PDT treatment decreased the expression of FoxO6 protein, promoted oxidative stress in HKFs, up-regulated ROS and MDA levels in HKFs and reduced SOD and CAT antioxidant enzyme activities. In addition, 5-ALA-PDT pretreatment increased the level of cell cycle-associated protein Cyclin D1, decreased the levels of Cyclin A1 and Cyclin B1, and accelerated cell cycle arrest in the G<sub>0</sub>/G<sub>1</sub> phase of HKFs. Overexpression of FoxO6 partially annulled the promoting effects of 5-ALA-PDT on G<sub>0</sub>/G<sub>1</sub> phase cell cycle arrest and oxidative stress in HKFs and enhanced cell proliferation and invasion.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>5-ALA-PDT limited HKF proliferation and invasion by down-regulating the expression of FoxO6.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"13 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138560003","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

Long noncoding RNA MAFG-AS1 enhances proliferation, invasion, and epithelial–mesenchymal transition of melanoma cells through promoting KIT expression by competitively binding to miR-331-3p 长非编码 RNA MAFG-AS1 通过与 miR-331-3p 竞争性结合，促进 KIT 的表达，从而增强黑色素瘤细胞的增殖、侵袭和上皮-间质转化能力

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-12-07 DOI: 10.1007/s13273-023-00409-3

Zongjiang Yao, Peiwu Li, Hong Liu

{"title":"Long noncoding RNA MAFG-AS1 enhances proliferation, invasion, and epithelial–mesenchymal transition of melanoma cells through promoting KIT expression by competitively binding to miR-331-3p","authors":"Zongjiang Yao, Peiwu Li, Hong Liu","doi":"10.1007/s13273-023-00409-3","DOIUrl":"https://doi.org/10.1007/s13273-023-00409-3","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Objective</h3><p>Melanoma is a malignant skin cancer. This paper is dedicated to investigate the disease mechanism in regard to the axis of long noncoding RNA MAFG antisense 1 (MAFG-AS1)/microRNA (miR)-331-3p/KIT.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Levels of MAFG-AS1, miR-331-3p and KIT were analyzed in melanoma patients' cancer tissues and melanocytic nevi patients’ skin tissues. The correlation between prognosis of melanoma patients with MAFG-AS1 expression was observed. Loss- and gain-function tests were implemented to observe alternatives of cell biological activities.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Melanoma patients’ cancer tissues expressed higher MAFG-AS1 and KIT and lower miR-331-3p. Patients with high MAFG-AS1 expression exhibited a poorer prognosis. After down-regulating MAFG-AS1 in A375 cells, cell proliferation, invasiveness, epithelial–mesenchymal transition (EMT) decreased, and apoptosis increased. Up-regulating MAFG-AS1 caused the opposite consequences. miR-331-3p inhibition or KIT overexpression eliminated the blockade of proliferation, invasion, and EMT caused by MAFG-AS1 silencing.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>MAFG-AS1 competitively binds to miR-331-3p to elevate KIT expression, thereby enhancing the aggressiveness of melanoma cells.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"138 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138560660","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

Impact of diesel particulate matter on the olfactory bulb of mice: insights from behavioral, histological, and molecular assessments 柴油颗粒物质对小鼠嗅球的影响:来自行为、组织学和分子评估的见解

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-12-01 DOI: 10.1007/s13273-023-00414-6

Jeongmin Lee, Poornima D. E. Weerasinghe-Mudiyanselage, Bohye Kim, Sohi Kang, Joong-Sun Kim, Changjong Moon

{"title":"Impact of diesel particulate matter on the olfactory bulb of mice: insights from behavioral, histological, and molecular assessments","authors":"Jeongmin Lee, Poornima D. E. Weerasinghe-Mudiyanselage, Bohye Kim, Sohi Kang, Joong-Sun Kim, Changjong Moon","doi":"10.1007/s13273-023-00414-6","DOIUrl":"https://doi.org/10.1007/s13273-023-00414-6","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Diesel particulate matter (DPM) constitutes a significant air pollutant that adversely affects neurological health through the olfactory pathway. Although extensive human epidemiological and animal research exists, the specific mechanisms underlying DPM-induced olfactory dysfunction have not been definitively elucidated.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This study aimed to conduct a comprehensive analysis of the behavioral, histological, and molecular changes in the olfactory bulb (OB) of mice following intranasal exposure to 10 mg/kg DPM for a duration of four weeks.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Exposure to DPM led to notable olfactory impairment in the mice, characterized by an elevation in Iba-1-positive microglia, though without inducing neuronal cell death. Transcriptomic evaluation revealed 84 differentially expressed genes (DEGs) in the OB that met the criteria of fold change greater than 1.5 and a <i>p</i> value less than 0.05. Within this set, 55 genes were upregulated and 29 were downregulated. Gene ontology-based functional analysis revealed that these DEGs were primarily related to sensory organ morphogenesis, energy homeostasis, and the regulation of monocyte aggregation. Subsequent investigation using the Kyoto Encyclopedia of Genes and Genomes database identified enriched pathways connected to neuroactive ligand-receptor interactions and calcium signaling.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Our findings suggest a plausible association between DPM-induced olfactory dysfunction and disruptions in a range of molecular pathways. This hypothesis is supported by observed alterations in gene expression and the presence of mild neuroinflammation, primarily driven by microglial activation.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"58 2-3","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138513829","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

Silibinin alleviates DNA damage, mitochondrial dysfunction, and apoptosis caused by oxidative stress in human retinal pigment epithelial cells 水飞蓟宾可减轻氧化应激引起的人视网膜色素上皮细胞DNA损伤、线粒体功能障碍和细胞凋亡

IF 1.7 4区医学

Molecular & Cellular Toxicology Pub Date : 2023-11-25 DOI: 10.1007/s13273-023-00412-8

Yung Hyun Choi

{"title":"Silibinin alleviates DNA damage, mitochondrial dysfunction, and apoptosis caused by oxidative stress in human retinal pigment epithelial cells","authors":"Yung Hyun Choi","doi":"10.1007/s13273-023-00412-8","DOIUrl":"https://doi.org/10.1007/s13273-023-00412-8","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Silibinin, a flavonolignan, is known to have a variety of pharmacological activities, including antioxidant activity, but its antioxidant mechanism in the eye is unclear.</p><h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This study aimed to evaluate whether silibinin could protect human retinal pigment epithelial ARPE-19 cells from oxidative injury.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Silibinin attenuated cell viability reduction and DNA damage in ARPE-19 cells treated with hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), while inhibiting intracellular reactive oxygen species (ROS) production and preserving diminished glutathione (GSH). Silibinin also antagonized H<sub>2</sub>O<sub>2</sub>-induced inhibition of the expression and activity of antioxidant enzymes, such as GSH peroxidase and manganese superoxide dismutase, which was associated with inhibition of mitochondrial ROS production. Moreover, silibinin rescued ARPE-19 cells from H<sub>2</sub>O<sub>2</sub>-induced apoptosis by restoring the reduced Bcl-2/Bax ratio and reducing caspase-3 activation. In addition, silibinin suppressed the release of mitochondrial cytochrome <i>c</i> into the cytoplasm, which was achieved by interfering with mitochondrial membrane disruption.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>These findings imply that silibinin has potent ROS scavenging activity with the potential to protect against oxidative stress-mediated ocular diseases.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"14 3","pages":""},"PeriodicalIF":1.7,"publicationDate":"2023-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138513843","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}

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