(-)-Asarinin alleviates gastric precancerous lesions by promoting mitochondrial ROS accumulation and inhibiting the STAT3 signaling pathway

(-)-Asarinin (Asarinin) is the primary component in the extract of the herb Asarum sieboldii Miq. It possesses various functions, including pain relief, anti-viral and anti-tuberculous bacilli effects, and inhibition of tumor growth. Gastric precancerous lesion (GPL) is a common but potentially carc...

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Veröffentlicht in:Phytomedicine (Stuttgart) 2024-04, Vol.126, p.155348-155348, Article 155348
Hauptverfasser: Zhao, Maoyuan, Wen, Yueqiang, Yang, Yi, Pan, Huafeng, Xie, Shunkai, Shen, Caifei, Liao, Wenhao, Chen, Nianzhi, Zheng, Qiao, Zhang, Gang, Li, Yuchen, Gong, Daoyin, Tang, Jianyuan, Zhao, Ziyi, Zeng, Jinhao
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container_title Phytomedicine (Stuttgart)
container_volume 126
creator Zhao, Maoyuan
Wen, Yueqiang
Yang, Yi
Pan, Huafeng
Xie, Shunkai
Shen, Caifei
Liao, Wenhao
Chen, Nianzhi
Zheng, Qiao
Zhang, Gang
Li, Yuchen
Gong, Daoyin
Tang, Jianyuan
Zhao, Ziyi
Zeng, Jinhao
description (-)-Asarinin (Asarinin) is the primary component in the extract of the herb Asarum sieboldii Miq. It possesses various functions, including pain relief, anti-viral and anti-tuberculous bacilli effects, and inhibition of tumor growth. Gastric precancerous lesion (GPL) is a common but potentially carcinogenic chronic gastrointestinal disease, and its progression can lead to gastric dysfunction and cancer development. However, the protective effects of asarinin against GPL and the underlying mechanisms remain unexplored. A premalignant cell model (methylnitronitrosoguanidine-induced malignant transformation of human gastric epithelial cell strain, MC cells) and a GPL animal model were established and then were treated with asarinin. The cytotoxic effect of asarinin was assessed using a CCK8 assay. Detection of intracellular reactive oxygen species (ROS) using DCFH-DA. Apoptosis in MC cells was evaluated using an annexin V-FITC/PI assay. We performed western blot analysis and immunohistochemistry (IHC) to analyze relevant markers, investigating the in vitro and in vivo therapeutic effects of asarinin on GPL and its intrinsic mechanisms. Our findings showed that asarinin inhibited MC cell proliferation, enhanced intracellular ROS levels, and induced cell apoptosis. Further investigations revealed that the pharmacological effects of asarinin on MC cells were blocked by the ROS scavenger N-acetylcysteine. IHC revealed a significant upregulation of phospho-signal transducer and activator of transcription 3 (p-STAT3) protein expression in human GPL tissues. In vitro, asarinin exerted its pro-apoptotic effects in MC cells by modulating the STAT3 signaling pathway. Agonists of STAT3 were able to abolish the effects of asarinin on MC cells. In vivo, asarinin induced ROS accumulation and inhibited the STAT3 pathway in gastric mucosa of mice, thereby halting and even reversing the development of GPL. Asarinin induces apoptosis and delays the progression of GPL by promoting mitochondrial ROS production, decreasing mitochondrial membrane potential (MMP), and inhibiting the STAT3 pathway. [Display omitted]
doi_str_mv 10.1016/j.phymed.2024.155348
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It possesses various functions, including pain relief, anti-viral and anti-tuberculous bacilli effects, and inhibition of tumor growth. Gastric precancerous lesion (GPL) is a common but potentially carcinogenic chronic gastrointestinal disease, and its progression can lead to gastric dysfunction and cancer development. However, the protective effects of asarinin against GPL and the underlying mechanisms remain unexplored. A premalignant cell model (methylnitronitrosoguanidine-induced malignant transformation of human gastric epithelial cell strain, MC cells) and a GPL animal model were established and then were treated with asarinin. The cytotoxic effect of asarinin was assessed using a CCK8 assay. Detection of intracellular reactive oxygen species (ROS) using DCFH-DA. Apoptosis in MC cells was evaluated using an annexin V-FITC/PI assay. We performed western blot analysis and immunohistochemistry (IHC) to analyze relevant markers, investigating the in vitro and in vivo therapeutic effects of asarinin on GPL and its intrinsic mechanisms. Our findings showed that asarinin inhibited MC cell proliferation, enhanced intracellular ROS levels, and induced cell apoptosis. Further investigations revealed that the pharmacological effects of asarinin on MC cells were blocked by the ROS scavenger N-acetylcysteine. IHC revealed a significant upregulation of phospho-signal transducer and activator of transcription 3 (p-STAT3) protein expression in human GPL tissues. In vitro, asarinin exerted its pro-apoptotic effects in MC cells by modulating the STAT3 signaling pathway. Agonists of STAT3 were able to abolish the effects of asarinin on MC cells. In vivo, asarinin induced ROS accumulation and inhibited the STAT3 pathway in gastric mucosa of mice, thereby halting and even reversing the development of GPL. Asarinin induces apoptosis and delays the progression of GPL by promoting mitochondrial ROS production, decreasing mitochondrial membrane potential (MMP), and inhibiting the STAT3 pathway. [Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2024.155348</identifier><identifier>PMID: 38335913</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>(-)-Asarinin ; Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Dioxoles ; Gastric precancerous lesions ; Humans ; Lignans - pharmacology ; Mice ; Mitochondria ; Precancerous Conditions - chemically induced ; Precancerous Conditions - drug therapy ; Precancerous Conditions - pathology ; Reactive Oxygen Species - metabolism ; ROS ; Signal Transduction ; STAT3 ; STAT3 Transcription Factor - metabolism</subject><ispartof>Phytomedicine (Stuttgart), 2024-04, Vol.126, p.155348-155348, Article 155348</ispartof><rights>2024 Elsevier GmbH</rights><rights>Copyright © 2024 Elsevier GmbH. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-1923ca55ee275337e314e256ce665041fba5221bcd6c4ec9cd8c4cf05e63fb8b3</citedby><cites>FETCH-LOGICAL-c362t-1923ca55ee275337e314e256ce665041fba5221bcd6c4ec9cd8c4cf05e63fb8b3</cites><orcidid>0000-0002-5860-3790</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.phymed.2024.155348$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38335913$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Maoyuan</creatorcontrib><creatorcontrib>Wen, Yueqiang</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Pan, Huafeng</creatorcontrib><creatorcontrib>Xie, Shunkai</creatorcontrib><creatorcontrib>Shen, Caifei</creatorcontrib><creatorcontrib>Liao, Wenhao</creatorcontrib><creatorcontrib>Chen, Nianzhi</creatorcontrib><creatorcontrib>Zheng, Qiao</creatorcontrib><creatorcontrib>Zhang, Gang</creatorcontrib><creatorcontrib>Li, Yuchen</creatorcontrib><creatorcontrib>Gong, Daoyin</creatorcontrib><creatorcontrib>Tang, Jianyuan</creatorcontrib><creatorcontrib>Zhao, Ziyi</creatorcontrib><creatorcontrib>Zeng, Jinhao</creatorcontrib><title>(-)-Asarinin alleviates gastric precancerous lesions by promoting mitochondrial ROS accumulation and inhibiting the STAT3 signaling pathway</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>(-)-Asarinin (Asarinin) is the primary component in the extract of the herb Asarum sieboldii Miq. It possesses various functions, including pain relief, anti-viral and anti-tuberculous bacilli effects, and inhibition of tumor growth. Gastric precancerous lesion (GPL) is a common but potentially carcinogenic chronic gastrointestinal disease, and its progression can lead to gastric dysfunction and cancer development. However, the protective effects of asarinin against GPL and the underlying mechanisms remain unexplored. A premalignant cell model (methylnitronitrosoguanidine-induced malignant transformation of human gastric epithelial cell strain, MC cells) and a GPL animal model were established and then were treated with asarinin. The cytotoxic effect of asarinin was assessed using a CCK8 assay. Detection of intracellular reactive oxygen species (ROS) using DCFH-DA. Apoptosis in MC cells was evaluated using an annexin V-FITC/PI assay. We performed western blot analysis and immunohistochemistry (IHC) to analyze relevant markers, investigating the in vitro and in vivo therapeutic effects of asarinin on GPL and its intrinsic mechanisms. Our findings showed that asarinin inhibited MC cell proliferation, enhanced intracellular ROS levels, and induced cell apoptosis. Further investigations revealed that the pharmacological effects of asarinin on MC cells were blocked by the ROS scavenger N-acetylcysteine. IHC revealed a significant upregulation of phospho-signal transducer and activator of transcription 3 (p-STAT3) protein expression in human GPL tissues. In vitro, asarinin exerted its pro-apoptotic effects in MC cells by modulating the STAT3 signaling pathway. Agonists of STAT3 were able to abolish the effects of asarinin on MC cells. In vivo, asarinin induced ROS accumulation and inhibited the STAT3 pathway in gastric mucosa of mice, thereby halting and even reversing the development of GPL. Asarinin induces apoptosis and delays the progression of GPL by promoting mitochondrial ROS production, decreasing mitochondrial membrane potential (MMP), and inhibiting the STAT3 pathway. [Display omitted]</description><subject>(-)-Asarinin</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Dioxoles</subject><subject>Gastric precancerous lesions</subject><subject>Humans</subject><subject>Lignans - pharmacology</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Precancerous Conditions - chemically induced</subject><subject>Precancerous Conditions - drug therapy</subject><subject>Precancerous Conditions - pathology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>ROS</subject><subject>Signal Transduction</subject><subject>STAT3</subject><subject>STAT3 Transcription Factor - metabolism</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQxi0EotvCGyDkYzlk8d9sfEFaVUCRKlWii8TNcpzJxivHWWynaJ-Bl8ZL2iunkWZ-M6Pv-xB6R8maElp_PKyPw2mEbs0IE2sqJRfNC7SiNW0qouTPl2hFlBDVhlJ-gS5TOhBChdqQ1-iCN5xLRfkK_bmuPlTbZKILLmDjPTw6kyHhvUk5OouPEawJFuI0J-whuSkk3J5Kfxqn7MIejy5PdphCF53x-Pv9AzbWzuPsTS4wNqHDLgyudf_oPAB-2G13HCe3D8afe0eTh9_m9Aa96o1P8PapXqEfXz7vbm6ru_uv3262d5XlNcsVVYxbIyUA20jON8CpACZrC3UtiaB9ayRjtLVdbQVYZbvGCtsTCTXv26blV-h6uVs0_JohZT26ZMF7E6Co1EwxoVQjiSqoWFAbp5Qi9PoY3WjiSVOizzHog15i0OcY9BJDWXv_9GFuz7PnpWffC_BpAaDofHQQdbIOis2dK35n3U3u_x_-AsCunak</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Zhao, Maoyuan</creator><creator>Wen, Yueqiang</creator><creator>Yang, Yi</creator><creator>Pan, Huafeng</creator><creator>Xie, Shunkai</creator><creator>Shen, Caifei</creator><creator>Liao, Wenhao</creator><creator>Chen, Nianzhi</creator><creator>Zheng, Qiao</creator><creator>Zhang, Gang</creator><creator>Li, Yuchen</creator><creator>Gong, Daoyin</creator><creator>Tang, Jianyuan</creator><creator>Zhao, Ziyi</creator><creator>Zeng, Jinhao</creator><general>Elsevier GmbH</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5860-3790</orcidid></search><sort><creationdate>202404</creationdate><title>(-)-Asarinin alleviates gastric precancerous lesions by promoting mitochondrial ROS accumulation and inhibiting the STAT3 signaling pathway</title><author>Zhao, Maoyuan ; Wen, Yueqiang ; Yang, Yi ; Pan, Huafeng ; Xie, Shunkai ; Shen, Caifei ; Liao, Wenhao ; Chen, Nianzhi ; Zheng, Qiao ; Zhang, Gang ; Li, Yuchen ; Gong, Daoyin ; Tang, Jianyuan ; Zhao, Ziyi ; Zeng, Jinhao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-1923ca55ee275337e314e256ce665041fba5221bcd6c4ec9cd8c4cf05e63fb8b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>(-)-Asarinin</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Dioxoles</topic><topic>Gastric precancerous lesions</topic><topic>Humans</topic><topic>Lignans - pharmacology</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Precancerous Conditions - chemically induced</topic><topic>Precancerous Conditions - drug therapy</topic><topic>Precancerous Conditions - pathology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>ROS</topic><topic>Signal Transduction</topic><topic>STAT3</topic><topic>STAT3 Transcription Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Maoyuan</creatorcontrib><creatorcontrib>Wen, Yueqiang</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Pan, Huafeng</creatorcontrib><creatorcontrib>Xie, Shunkai</creatorcontrib><creatorcontrib>Shen, Caifei</creatorcontrib><creatorcontrib>Liao, Wenhao</creatorcontrib><creatorcontrib>Chen, Nianzhi</creatorcontrib><creatorcontrib>Zheng, Qiao</creatorcontrib><creatorcontrib>Zhang, Gang</creatorcontrib><creatorcontrib>Li, Yuchen</creatorcontrib><creatorcontrib>Gong, Daoyin</creatorcontrib><creatorcontrib>Tang, Jianyuan</creatorcontrib><creatorcontrib>Zhao, Ziyi</creatorcontrib><creatorcontrib>Zeng, Jinhao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Maoyuan</au><au>Wen, Yueqiang</au><au>Yang, Yi</au><au>Pan, Huafeng</au><au>Xie, Shunkai</au><au>Shen, Caifei</au><au>Liao, Wenhao</au><au>Chen, Nianzhi</au><au>Zheng, Qiao</au><au>Zhang, Gang</au><au>Li, Yuchen</au><au>Gong, Daoyin</au><au>Tang, Jianyuan</au><au>Zhao, Ziyi</au><au>Zeng, Jinhao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>(-)-Asarinin alleviates gastric precancerous lesions by promoting mitochondrial ROS accumulation and inhibiting the STAT3 signaling pathway</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2024-04</date><risdate>2024</risdate><volume>126</volume><spage>155348</spage><epage>155348</epage><pages>155348-155348</pages><artnum>155348</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>(-)-Asarinin (Asarinin) is the primary component in the extract of the herb Asarum sieboldii Miq. It possesses various functions, including pain relief, anti-viral and anti-tuberculous bacilli effects, and inhibition of tumor growth. Gastric precancerous lesion (GPL) is a common but potentially carcinogenic chronic gastrointestinal disease, and its progression can lead to gastric dysfunction and cancer development. However, the protective effects of asarinin against GPL and the underlying mechanisms remain unexplored. A premalignant cell model (methylnitronitrosoguanidine-induced malignant transformation of human gastric epithelial cell strain, MC cells) and a GPL animal model were established and then were treated with asarinin. The cytotoxic effect of asarinin was assessed using a CCK8 assay. Detection of intracellular reactive oxygen species (ROS) using DCFH-DA. Apoptosis in MC cells was evaluated using an annexin V-FITC/PI assay. We performed western blot analysis and immunohistochemistry (IHC) to analyze relevant markers, investigating the in vitro and in vivo therapeutic effects of asarinin on GPL and its intrinsic mechanisms. Our findings showed that asarinin inhibited MC cell proliferation, enhanced intracellular ROS levels, and induced cell apoptosis. Further investigations revealed that the pharmacological effects of asarinin on MC cells were blocked by the ROS scavenger N-acetylcysteine. IHC revealed a significant upregulation of phospho-signal transducer and activator of transcription 3 (p-STAT3) protein expression in human GPL tissues. In vitro, asarinin exerted its pro-apoptotic effects in MC cells by modulating the STAT3 signaling pathway. Agonists of STAT3 were able to abolish the effects of asarinin on MC cells. In vivo, asarinin induced ROS accumulation and inhibited the STAT3 pathway in gastric mucosa of mice, thereby halting and even reversing the development of GPL. Asarinin induces apoptosis and delays the progression of GPL by promoting mitochondrial ROS production, decreasing mitochondrial membrane potential (MMP), and inhibiting the STAT3 pathway. [Display omitted]</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>38335913</pmid><doi>10.1016/j.phymed.2024.155348</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5860-3790</orcidid></addata></record>
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subjects (-)-Asarinin
Animals
Apoptosis
Cell Line, Tumor
Cell Proliferation
Dioxoles
Gastric precancerous lesions
Humans
Lignans - pharmacology
Mice
Mitochondria
Precancerous Conditions - chemically induced
Precancerous Conditions - drug therapy
Precancerous Conditions - pathology
Reactive Oxygen Species - metabolism
ROS
Signal Transduction
STAT3
STAT3 Transcription Factor - metabolism
title (-)-Asarinin alleviates gastric precancerous lesions by promoting mitochondrial ROS accumulation and inhibiting the STAT3 signaling pathway
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