Animal Cells and Systems最新文献_第10页

Emerging roles of cytoskeletal transport and scaffold systems in human viral propagation. 细胞骨架运输和支架系统在人类病毒传播中的新作用。

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-10-21 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2418332

Younghyun Lim, Yong-Bin Cho, Young-Jin Seo

{"title":"Emerging roles of cytoskeletal transport and scaffold systems in human viral propagation.","authors":"Younghyun Lim, Yong-Bin Cho, Young-Jin Seo","doi":"10.1080/19768354.2024.2418332","DOIUrl":"https://doi.org/10.1080/19768354.2024.2418332","url":null,"abstract":"Viruses have long been recognized as significant pathogens, contributing to multiple global pandemics throughout human history. Recent examples include the 2009 influenza pandemic and the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in 2019. Despite ongoing experimental and clinical efforts, the development of effective antiviral treatments and vaccines remains challenging due to the high mutation rates of many human pathogenic viruses including influenza virus and SARS-CoV-2. As an alternative approach, antiviral strategies targeting host factors shared by multiple viruses could provide a more universally applicable solution. Emerging evidence suggests that viruses exploit the host cytoskeletal network to facilitate efficient viral replication and propagation. Therefore, a comprehensive understanding of the interactions between viral components and the cytoskeletal machinery may offer valuable insights for the development of broad-spectrum antiviral therapeutics. This review compiles and discusses current knowledge on the interactions between viruses and cytoskeletal elements, including kinesin, dynein, myosin, and vimentin, and explores their potential as therapeutic targets. The potential for these cytoskeletal components to serve as targets for new antiviral interventions is discussed in the context of diverse human viruses, including influenza virus, SARS-CoV-2, herpes simplex virus, human papillomavirus, and human immunodeficiency virus.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"506-518"},"PeriodicalIF":2.5,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11494721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nitrogen-doped carbon quantum dot regulates cell proliferation and differentiation by endoplasmic reticulum stress. 掺氮碳量子点通过内质网应激调节细胞增殖和分化

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-10-02 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2409452

Hyun Hee Song, Hyunwoo Choi, Seonghan Kim, Hwan Gyu Kim, Sangmin An, Sejung Kim, Hoon Jang

{"title":"Nitrogen-doped carbon quantum dot regulates cell proliferation and differentiation by endoplasmic reticulum stress.","authors":"Hyun Hee Song, Hyunwoo Choi, Seonghan Kim, Hwan Gyu Kim, Sangmin An, Sejung Kim, Hoon Jang","doi":"10.1080/19768354.2024.2409452","DOIUrl":"10.1080/19768354.2024.2409452","url":null,"abstract":"Quantum dots have diverse biomedical applications, from constructing biological infrastructures like medical imaging to advancing pharmaceutical research. However, concerns about human health arise due to the toxic potential of quantum dots based on heavy metals. Therefore, research on quantum dots has predominantly focused on oxidative stress, cell death, and other broader bodily toxicities. This study investigated the toxicity and cellular responses of mouse embryonic stem cells (mESCs) and mouse adult stem cells (mASCs) to nitrogen-doped carbon quantum dots (NCQDs) made of non-metallic materials. Cells were exposed to NCQDs, and we utilized a fluorescent ubiquitination-based cell system to verify whether NCQDs induce cytotoxicity. Furthermore, we validated the differentiation-inducing impact of NCQDs by utilizing embryonic stem cells equipped with the Oct4 enhancer-GFP reporter system. By analyzing gene expression including Crebzf, Chop, and ATF6, we also observed that NCQDs robustly elicited endoplasmic reticulum (ER) stress. We confirmed that NCQDs induced cytotoxicity and abnormal differentiation. Interestingly, we also confirmed that low concentrations of NCQDs stimulated cell proliferation in both mESCs and mASCs. In conclusion, NCQDs modulate cell death, proliferation, and differentiation in a concentration-dependent manner. Indiscriminate biological applications of NCQDs have the potential to cause cancer development by affecting normal cell division or to fail to induce normal differentiation by affecting embryonic development during pregnancy. Therefore, we propose that future biomedical applications of NCQDs necessitate comprehensive and diverse biological studies.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"481-494"},"PeriodicalIF":2.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gender-specific alteration of steroid metabolism and its impact on viral replication in a mouse model of hepatitis B virus infection. 乙型肝炎病毒感染小鼠模型中类固醇代谢的性别特异性改变及其对病毒复制的影响。

IF 2.9 2区生物学

Animal Cells and Systems Pub Date : 2024-09-17 DOI: 10.1080/19768354.2024.2403569

Eun-Sook Park,Juhee Won,Sung Hyun Ahn,Ah Ram Lee,Donghyo Lee,Ju-Yeon Moon,Man Ho Choi,Kyun-Hwan Kim

{"title":"Gender-specific alteration of steroid metabolism and its impact on viral replication in a mouse model of hepatitis B virus infection.","authors":"Eun-Sook Park,Juhee Won,Sung Hyun Ahn,Ah Ram Lee,Donghyo Lee,Ju-Yeon Moon,Man Ho Choi,Kyun-Hwan Kim","doi":"10.1080/19768354.2024.2403569","DOIUrl":"https://doi.org/10.1080/19768354.2024.2403569","url":null,"abstract":"Hepatitis B virus (HBV) is a sex-specific pathogen that is more severe in males than in females. Sex disparities in HBV infection have been attributed to hormonal differences between males and females. However, whether HBV infection affects the metabolic signatures of steroid hormones and how these influences viral replication remains unclear. In this study, we investigated whether HBV infection alters steroid metabolism and its effects on HBV replication. Serum samples from male and female mice obtained after the hydrodynamic injection of replication-competent HBV plasmids were subjected to quantitative steroid profiling. Serum steroid levels in mice were analyzed using an in vitro metabolism assay with the mouse liver S9 fraction. The alteration of steroids by HBV infection was observed only in male mice, particularly with significant changes in androgens, whereas no significant hormonal changes were observed in female mice. Among the altered steroids, dehydroepiandrosterone (DHEA) levels increased the most in male mice after HBV infection. An in vitro metabolism assay revealed that androgen levels were significantly reduced in HBV-infected male mice. Furthermore, the genes involved in DHEA biosynthesis were significantly upregulated in HBV-infected male mice. Interestingly, reduced dihydrotestosterone in male mice significantly inhibits viral replication by suppressing HBV promoter activity, suggesting a viral strategy to overcome the antiviral effects of steroid hormones in males. Our data demonstrated that HBV infection can cause sex-specific changes in steroid metabolism.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"35 1","pages":"466-480"},"PeriodicalIF":2.9,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of maternal nonylphenol exposure on the proliferation of glial cells in the brain of male offspring mice. 母体接触壬基酚对雄性后代小鼠大脑胶质细胞增殖的影响

IF 2.9 2区生物学

Animal Cells and Systems Pub Date : 2024-09-12 DOI: 10.1080/19768354.2024.2401389

Seung Hyun Lee,Hyun Seung Shin,Yun Hee So,Dong Hun Lee,Jin Yeop Kim,Eun-Hee Lee,Eui-Man Jung

{"title":"Effects of maternal nonylphenol exposure on the proliferation of glial cells in the brain of male offspring mice.","authors":"Seung Hyun Lee,Hyun Seung Shin,Yun Hee So,Dong Hun Lee,Jin Yeop Kim,Eun-Hee Lee,Eui-Man Jung","doi":"10.1080/19768354.2024.2401389","DOIUrl":"https://doi.org/10.1080/19768354.2024.2401389","url":null,"abstract":"Glial cells play a significant role in maintaining brain homeostasis and normal brain development, and their functions can be impaired by exposure to endocrine disruptors. 4-n-Nonylphenol (NP), a representative endocrine disruptor, is widely used in personal care products and industrial materials. NP accumulates in various organs, including the brain, of living organisms and adversely influences brain health. However, studies on the effects of NP on glial cells are limited. This study aims to investigate the effects of NP on glial cells using primary mixed glial cells and offspring mice exposed to NP during gestation and lactation. In vitro experiments revealed that NP exposure stimulated the astrocytes and microglia proliferation but not oligodendrocytes. NP exposure activated microglia and reduced myelin protein expression in oligodendrocytes. Moreover, maternal NP exposure increased the numbers of microglia and oligodendrocytes in the cerebral cortex of adult offspring. NP exposure caused anxiety- and depressive-like behaviors in adult mice. Collectively, these findings suggest that maternal NP exposure negatively affects the brain development in adult offspring mice.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"30 1","pages":"439-452"},"PeriodicalIF":2.9,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CXCL10 promotes melanoma angiogenesis and tumor growth CXCL10 促进黑色素瘤血管生成和肿瘤生长

IF 2.9 2区生物学

Animal Cells and Systems Pub Date : 2024-09-11 DOI: 10.1080/19768354.2024.2402024

Bongjun Kim, Yun-Yong Park, Jong-Ho Lee

引用次数: 0

Low-temperature pulverization-specific Sargassum horneri extract accelerates wound healing and attenuates inflammation in a mouse burn model. 低温粉碎特异性马尾藻提取物可加速小鼠烧伤模型的伤口愈合并减轻炎症反应。

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2396903

Eunguk Shin, Hee-Tae Kim, Haksoo Lee, Byeongsoo Kim, Junhyeong Park, Sujin Park, Soomin Yum, Seul-Kee Kim, Jae-Myung Lee, BuHyun Youn

{"title":"Low-temperature pulverization-specific Sargassum horneri extract accelerates wound healing and attenuates inflammation in a mouse burn model.","authors":"Eunguk Shin, Hee-Tae Kim, Haksoo Lee, Byeongsoo Kim, Junhyeong Park, Sujin Park, Soomin Yum, Seul-Kee Kim, Jae-Myung Lee, BuHyun Youn","doi":"10.1080/19768354.2024.2396903","DOIUrl":"10.1080/19768354.2024.2396903","url":null,"abstract":"Burn injuries, affecting local skin disruption as well as inducing systemic inflammatory responses, are presented as a global public health problem. To enhance the effects of burn wound healing, treatment must simultaneously regulate both re-epithelialization and hyperinflammation. Extracts of Sargassum horneri (S. horneri) have shown a potential to enhance skin wound healing through antioxidative properties, immune enhancement, and modulation of inflammatory responses. However, despite its promising application for burn wound healing, specific investigation into S. horneri-derived compounds for enhancing wound healing has not yet been conducted. In this research, we investigated the burn wound-healing effect of the low-temperature pulverization-specific S. horneri extract (LPSHE), which could not be detected using the room-temperature grinding method. In a mouse burn model with third-degree burn injuries, LPSHE accelerated re-epithelialization by promoting the increase in F-actin formation and reduced burn-induced ROS levels. Additionally, LPSHE significantly regulated hyperinflammation by reducing pro-inflammatory cytokines. Further investigation into molecular mechanisms using HaCaT keratinocytes also demonstrated beneficial effects on burn wound healing. Taken together, our findings suggested that LPSHE is a promising therapeutic candidate for enhancing burn wound healing. Furthermore, this research underscored the importance of low-temperature pulverization in discovering novel natural compounds from marine organisms.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"428-438"},"PeriodicalIF":2.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142152987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ECM stiffness regulates calcium influx into mitochondria via tubulin and VDAC1 activity. ECM 硬度通过微管蛋白和 VDAC1 的活性调节线粒体的钙离子流入。

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-08-29 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2393811

Minji Kim, Kiseok Han, Gyuho Choi, Sanghyun Ahn, Jung-Soo Suh, Tae-Jin Kim

{"title":"ECM stiffness regulates calcium influx into mitochondria via tubulin and VDAC1 activity.","authors":"Minji Kim, Kiseok Han, Gyuho Choi, Sanghyun Ahn, Jung-Soo Suh, Tae-Jin Kim","doi":"10.1080/19768354.2024.2393811","DOIUrl":"10.1080/19768354.2024.2393811","url":null,"abstract":"Calcium ions (Ca2+) play pivotal roles in regulating numerous cellular functions, including metabolism and growth, in normal and cancerous cells. Consequently, Ca2+ signaling is a vital determinant of cell fate and influences both cell survival and death. These intracellular signals are susceptible to modulation by various factors, including changes in the extracellular environment, which leads to mechanical alterations. However, the effect of extracellular matrix (ECM) stiffness variations on intracellular Ca2+ signaling remains underexplored. In this study, we aimed to elucidate the mechanisms of Ca2+ regulation through the mitochondria, which are crucial to Ca2+ homeostasis. We investigated how Ca2+ regulatory mechanisms adapt to different levels of ECM stiffness by simultaneously imaging the mitochondria and endoplasmic reticulum (ER) in live cells using genetically encoded biosensors. Our findings revealed that the uptake of mitochondrial Ca2+ through Voltage-Dependent Anion Channel 1 (VDAC1), facilitated by intracellular tubulin, is influenced by ECM stiffness. Unraveling these Ca2+ regulatory mechanisms under various conditions offers a novel perspective for advancing biomedical studies involving Ca2+ signaling.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"417-427"},"PeriodicalIF":2.5,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11363740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways. Lamin A/C 通过调节 ATM 信号和同源重组途径促进 DNA 损伤反应。

IF 3.6 2区生物学

Animal Cells and Systems Pub Date : 2024-08-20 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2393820

Seong-Jung Kim, Su Hyung Park, Kyungjae Myung, Kyoo-Young Lee

{"title":"Lamin A/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways.","authors":"Seong-Jung Kim, Su Hyung Park, Kyungjae Myung, Kyoo-Young Lee","doi":"10.1080/19768354.2024.2393820","DOIUrl":"10.1080/19768354.2024.2393820","url":null,"abstract":"Lamin A/C, a core component of the nuclear lamina, forms a mesh-like structure beneath the inner nuclear membrane. While its structural role is well-studied, its involvement in DNA metabolism remains unclear. We conducted sequential protein fractionation to determine the subcellular localization of early DNA damage response (DDR) proteins. Our findings indicate that most DDR proteins, including ATM and the MRE11-RAD50-NBS1 (MRN) complex, are present in the nuclease - and high salt-resistant pellet fraction. Notably, ATM and MRN remain stably associated with these structures throughout the cell cycle, independent of ionizing radiation (IR)-induced DNA damage. Although Lamin A/C interacts with ATM and MRN, its depletion does not disrupt their association with nuclease-resistant structures. However, it impairs the IR-enhanced association of ATM with the nuclear matrix and ATM-mediated DDR signaling, as well as the interaction between ATM and MRN. This disruption impedes the recruitment of MRE11 to damaged DNA and the association of damaged DNA with the nuclear matrix. Additionally, Lamin A/C depletion results in reduced protein levels of CtIP and RAD51, which is mediated by transcriptional regulation. This, in turn, impairs the efficiency of homologous recombination (HR). Our findings indicate that Lamin A/C plays a pivotal role in DNA damage repair (DDR) by orchestrating ATM-mediated signaling, maintaining HR protein levels, and ensuring efficient DNA repair processes.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"401-416"},"PeriodicalIF":3.6,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11340224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142034950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Licochalcone A attenuates NMDA-induced neurotoxicity. 甘草查尔酮 A 可减轻 NMDA 诱导的神经毒性。

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-08-12 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2389823

Jae Soo Kim, Mi-Hye Kim, Myeung Ju Kim, Hee Jung Kim

{"title":"Licochalcone A attenuates NMDA-induced neurotoxicity.","authors":"Jae Soo Kim, Mi-Hye Kim, Myeung Ju Kim, Hee Jung Kim","doi":"10.1080/19768354.2024.2389823","DOIUrl":"10.1080/19768354.2024.2389823","url":null,"abstract":"This study investigates the effect of Licochalcone A (Lico-A), a flavonoid from licorice roots known for its anti-inflammatory, anti-cancer, and antioxidant properties, on NMDA-induced neurotoxicity in primary cultured rat hippocampal neurons. The study measured cell survival following NMDA and Lico-A exposure, revealing that Lico-A at a 2.5 μg/ml significantly improved cell viability, countering the detrimental effects of NMDA. The study also analyzed synaptic changes by examining both postsynaptic density 95 (PSD95) and synaptophysin-targeted imaging, showing that Lico-A treatment resulted in a significant increase in synaptic puncta, contrasting with the reduction observed under NMDA exposure. Furthermore, levels of phosphorylated mixed lineage kinase domain-like pseudokinase (P-MLKL) and phosphorylated receptor-interacting serine/threonine-protein kinase 3 (P-RIP3), key necroptosis regulators, were measured using Western blotting. The results showed an increase in P-MLKL and P-RIP3 in neurons exposed to NMDA, which was reduced following Lico-A treatment. The response of astrocyte and microglia was also evaluated by immunostaining for glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor molecule 1 (IBA-1) and tumor necrosis factor alpha (TNF-α). These markers exhibited heightened expression in the NMDA group, which was substantially reduced by Lico-A treatment. These findings suggest that Lico-A has neuroprotective effects against NMDA-induced neurotoxicity, potentially contributing to synaptic preservation, inhibition of neuronal necroptosis, and modulation of glial activation. Therefore, Lico-A shows promise as a neuroprotective agent for conditions associated with NMDA-related neurotoxicity.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"392-400"},"PeriodicalIF":2.5,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141977624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Camellia sinensis L. alleviates OVA-induced allergic asthma through NF-κB and MMP-9 pathways. 山茶通过NF-κB和MMP-9途径缓解OVA诱导的过敏性哮喘

IF 2.5 2区生物学

Animal Cells and Systems Pub Date : 2024-08-01 eCollection Date: 2024-01-01 DOI: 10.1080/19768354.2024.2383254

So-Won Pak, Ik Soo Lee, Woong-Il Kim, Se-Jin Lee, Jong-Choon Kim, In-Sik Shin, Taesoo Kim

{"title":"Camellia sinensis L. alleviates OVA-induced allergic asthma through NF-κB and MMP-9 pathways.","authors":"So-Won Pak, Ik Soo Lee, Woong-Il Kim, Se-Jin Lee, Jong-Choon Kim, In-Sik Shin, Taesoo Kim","doi":"10.1080/19768354.2024.2383254","DOIUrl":"10.1080/19768354.2024.2383254","url":null,"abstract":"Allergic asthma, a type of chronic airway inflammation, is a global health concern because of its increasing incidence and recurrence rates. Camellia sinensis L. yields a variety type of teas, which are also used as medicinal plants in East Asia and are known to have antioxidant, anti-inflammatory, and immune-potentiating properties. Here, we examined the constituents of C. sinensis L. extract (CSE) and evaluated the protective effects of CSE on allergic asthma by elucidating the underlying mechanism. To induce allergic asthma, we injected the sensitization solution (mixture of ovalbumin (OVA) and aluminum hydroxide) into mice intraperitoneally on days 0 and 14. Then, the mice were exposed to 1% OVA by a nebulizer on days 21 to 23, while intragastric administration of CSE (30 and 100 mg/kg) was performed each day on days 18 to 23. We detected five compounds in CSE, including (-)-epigallocatechin, caffeine, (-)-epicatechin, (-)-epigallocatechin gallate, and (-)-epicatechin gallate. Treatment with CSE remarkably decreased the airway hyperresponsiveness, OVA-specific immunoglobulin E level, and inflammatory cell and cytokine levels of mice, with a decrease in inflammatory cell infiltration and mucus production in lung tissue. Treatment with CSE also decreased the phosphorylation of nuclear factor-κB (NF-κB) and the expression of matrix-metalloproteinase (MMP)-9 in asthmatic mice. Our results demonstrated that CSE reduced allergic airway inflammation caused by OVA through inhibition of phosphorylated NF-κB and MMP-9 expression.","PeriodicalId":7804,"journal":{"name":"Animal Cells and Systems","volume":"28 1","pages":"381-391"},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11295686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0