Cannabidiol ameliorates inflammatory response partly by AGE-RAGE pathway in diabetic mice
Cannabidiol (CBD), the most abundant nonpsychoactive constituent of Cannabis sativa plant, is a promising potential pharmacotherapy for the treatment of diabetes and associated comorbidities. Previous studies have shown the potential of CBD to prevent diabetes in mice, the precise mechanisms of acti...
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| Veröffentlicht in: | Drug development research 2023-11, Vol.84 (7), p.1427-1436 |
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| container_title | Drug development research |
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| creator | Li, Shuai Fan, Chunxiang Li, Xu Li, Shanshan Yu, Tianfei Zhang, Weiwei Ma, Tianyi Zhao, Ming Li, Deshan Xiao, Wei Shan, Shanan |
| description | Cannabidiol (CBD), the most abundant nonpsychoactive constituent of Cannabis sativa plant, is a promising potential pharmacotherapy for the treatment of diabetes and associated comorbidities. Previous studies have shown the potential of CBD to prevent diabetes in mice, the precise mechanisms of action remain unclear. The purpose of this study was to explore the mechanism of CBD alleviating hyperglycemia. The results demonstrated that CBD reduced blood glucose of STZ-induced diabetic mice without causing hypoglycemia. To elucidate the possible mechanisms of CBD effect, RNA-seq analysis was performed on high glucose-induced human mesangial cells (HMCs). By cluster analysis of differential genes, the results showed that advanced glycation end products-receptor of advanced glycation endproducts (AGE-RAGE) pathway-related genes CCL2 and interleukin-1β (IL-1β) play an important role in the biological of CBD. The expression of CCL2 and IL-1β were significantly increased in HMCs. Whereas, treatment with CBD decreased the expression of CCL2 and IL-1β. In addition, CBD significantly reduced AGE-RAGE levels in high glucose-induced HMCs. Similar results were confirmed in diabetic mice. In conclusion, we discovered for the first time that CBD ameliorates hyperglycemia partly through AGE-RAGE mediated CCL2/IL-1β pathway. |
| doi_str_mv | 10.1002/ddr.22093 |
| format | Article |
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Previous studies have shown the potential of CBD to prevent diabetes in mice, the precise mechanisms of action remain unclear. The purpose of this study was to explore the mechanism of CBD alleviating hyperglycemia. The results demonstrated that CBD reduced blood glucose of STZ-induced diabetic mice without causing hypoglycemia. To elucidate the possible mechanisms of CBD effect, RNA-seq analysis was performed on high glucose-induced human mesangial cells (HMCs). By cluster analysis of differential genes, the results showed that advanced glycation end products-receptor of advanced glycation endproducts (AGE-RAGE) pathway-related genes CCL2 and interleukin-1β (IL-1β) play an important role in the biological of CBD. The expression of CCL2 and IL-1β were significantly increased in HMCs. Whereas, treatment with CBD decreased the expression of CCL2 and IL-1β. In addition, CBD significantly reduced AGE-RAGE levels in high glucose-induced HMCs. Similar results were confirmed in diabetic mice. In conclusion, we discovered for the first time that CBD ameliorates hyperglycemia partly through AGE-RAGE mediated CCL2/IL-1β pathway.</description><identifier>ISSN: 0272-4391</identifier><identifier>EISSN: 1098-2299</identifier><identifier>DOI: 10.1002/ddr.22093</identifier><identifier>PMID: 37486107</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Advanced glycosylation end products ; Age ; Cannabidiol ; Cannabinoids ; Cannabis ; Cluster analysis ; Comorbidity ; Diabetes ; Diabetes mellitus ; Drug therapy ; Genes ; Glucose ; Glycosylation ; Hyperglycemia ; Hypoglycemia ; Inflammation ; Inflammatory response ; Mesangial cells ; Monocyte chemoattractant protein 1</subject><ispartof>Drug development research, 2023-11, Vol.84 (7), p.1427-1436</ispartof><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c273t-31a5b2c8cb558b240c06b113bc3a6530b13a35f1f9fac9ffdc738cf0a6bf11763</cites><orcidid>0000-0003-1977-1035</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37486107$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shuai</creatorcontrib><creatorcontrib>Fan, Chunxiang</creatorcontrib><creatorcontrib>Li, Xu</creatorcontrib><creatorcontrib>Li, Shanshan</creatorcontrib><creatorcontrib>Yu, Tianfei</creatorcontrib><creatorcontrib>Zhang, Weiwei</creatorcontrib><creatorcontrib>Ma, Tianyi</creatorcontrib><creatorcontrib>Zhao, Ming</creatorcontrib><creatorcontrib>Li, Deshan</creatorcontrib><creatorcontrib>Xiao, Wei</creatorcontrib><creatorcontrib>Shan, Shanan</creatorcontrib><title>Cannabidiol ameliorates inflammatory response partly by AGE-RAGE pathway in diabetic mice</title><title>Drug development research</title><addtitle>Drug Dev Res</addtitle><description>Cannabidiol (CBD), the most abundant nonpsychoactive constituent of Cannabis sativa plant, is a promising potential pharmacotherapy for the treatment of diabetes and associated comorbidities. Previous studies have shown the potential of CBD to prevent diabetes in mice, the precise mechanisms of action remain unclear. The purpose of this study was to explore the mechanism of CBD alleviating hyperglycemia. The results demonstrated that CBD reduced blood glucose of STZ-induced diabetic mice without causing hypoglycemia. To elucidate the possible mechanisms of CBD effect, RNA-seq analysis was performed on high glucose-induced human mesangial cells (HMCs). By cluster analysis of differential genes, the results showed that advanced glycation end products-receptor of advanced glycation endproducts (AGE-RAGE) pathway-related genes CCL2 and interleukin-1β (IL-1β) play an important role in the biological of CBD. The expression of CCL2 and IL-1β were significantly increased in HMCs. Whereas, treatment with CBD decreased the expression of CCL2 and IL-1β. In addition, CBD significantly reduced AGE-RAGE levels in high glucose-induced HMCs. Similar results were confirmed in diabetic mice. In conclusion, we discovered for the first time that CBD ameliorates hyperglycemia partly through AGE-RAGE mediated CCL2/IL-1β pathway.</description><subject>Advanced glycosylation end products</subject><subject>Age</subject><subject>Cannabidiol</subject><subject>Cannabinoids</subject><subject>Cannabis</subject><subject>Cluster analysis</subject><subject>Comorbidity</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Drug therapy</subject><subject>Genes</subject><subject>Glucose</subject><subject>Glycosylation</subject><subject>Hyperglycemia</subject><subject>Hypoglycemia</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Mesangial cells</subject><subject>Monocyte chemoattractant protein 1</subject><issn>0272-4391</issn><issn>1098-2299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkE1LxDAQhoMouq4e_ANS8KKHrpmkbdKjLOsHCILowVOZpAlG2mZNukj_vdFVD15mYHjel-Eh5AToAihll20bFozRmu-QGdBa5ozV9S6ZUSZYXvAaDshhjG-UAhRS7pMDLgpZARUz8rLEYUDlWue7DHvTOR9wNDFzg-2w73H0YcqCiWs_RJOtMYzdlKkpu7pZ5Y9ppNP4-oFTCmStQ2VGp7PeaXNE9ix20Rz_7Dl5vl49LW_z-4ebu-XVfa6Z4GPOAUvFtNSqLKViBdW0UgBcaY5VyakCjry0YGuLura21YJLbSlWygKIis_J-bZ3Hfz7xsSx6V3UputwMH4TGyYLKGhZCJ7Qs3_om9-EIX2XKCmgElVZJ-piS-ngYwzGNuvgegxTA7T58t0k382378Se_jRuVG_aP_JXMP8E6hZ6gg</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Li, Shuai</creator><creator>Fan, Chunxiang</creator><creator>Li, Xu</creator><creator>Li, Shanshan</creator><creator>Yu, Tianfei</creator><creator>Zhang, Weiwei</creator><creator>Ma, Tianyi</creator><creator>Zhao, Ming</creator><creator>Li, Deshan</creator><creator>Xiao, Wei</creator><creator>Shan, Shanan</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-1977-1035</orcidid></search><sort><creationdate>20231101</creationdate><title>Cannabidiol ameliorates inflammatory response partly by AGE-RAGE pathway in diabetic mice</title><author>Li, Shuai ; Fan, Chunxiang ; Li, Xu ; Li, Shanshan ; Yu, Tianfei ; Zhang, Weiwei ; Ma, Tianyi ; Zhao, Ming ; Li, Deshan ; Xiao, Wei ; Shan, Shanan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c273t-31a5b2c8cb558b240c06b113bc3a6530b13a35f1f9fac9ffdc738cf0a6bf11763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Advanced glycosylation end products</topic><topic>Age</topic><topic>Cannabidiol</topic><topic>Cannabinoids</topic><topic>Cannabis</topic><topic>Cluster analysis</topic><topic>Comorbidity</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Drug therapy</topic><topic>Genes</topic><topic>Glucose</topic><topic>Glycosylation</topic><topic>Hyperglycemia</topic><topic>Hypoglycemia</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Mesangial cells</topic><topic>Monocyte chemoattractant protein 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shuai</creatorcontrib><creatorcontrib>Fan, Chunxiang</creatorcontrib><creatorcontrib>Li, Xu</creatorcontrib><creatorcontrib>Li, Shanshan</creatorcontrib><creatorcontrib>Yu, Tianfei</creatorcontrib><creatorcontrib>Zhang, Weiwei</creatorcontrib><creatorcontrib>Ma, Tianyi</creatorcontrib><creatorcontrib>Zhao, Ming</creatorcontrib><creatorcontrib>Li, Deshan</creatorcontrib><creatorcontrib>Xiao, Wei</creatorcontrib><creatorcontrib>Shan, Shanan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Drug development research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shuai</au><au>Fan, Chunxiang</au><au>Li, Xu</au><au>Li, Shanshan</au><au>Yu, Tianfei</au><au>Zhang, Weiwei</au><au>Ma, Tianyi</au><au>Zhao, Ming</au><au>Li, Deshan</au><au>Xiao, Wei</au><au>Shan, Shanan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cannabidiol ameliorates inflammatory response partly by AGE-RAGE pathway in diabetic mice</atitle><jtitle>Drug development research</jtitle><addtitle>Drug Dev Res</addtitle><date>2023-11-01</date><risdate>2023</risdate><volume>84</volume><issue>7</issue><spage>1427</spage><epage>1436</epage><pages>1427-1436</pages><issn>0272-4391</issn><eissn>1098-2299</eissn><abstract>Cannabidiol (CBD), the most abundant nonpsychoactive constituent of Cannabis sativa plant, is a promising potential pharmacotherapy for the treatment of diabetes and associated comorbidities. Previous studies have shown the potential of CBD to prevent diabetes in mice, the precise mechanisms of action remain unclear. The purpose of this study was to explore the mechanism of CBD alleviating hyperglycemia. The results demonstrated that CBD reduced blood glucose of STZ-induced diabetic mice without causing hypoglycemia. To elucidate the possible mechanisms of CBD effect, RNA-seq analysis was performed on high glucose-induced human mesangial cells (HMCs). By cluster analysis of differential genes, the results showed that advanced glycation end products-receptor of advanced glycation endproducts (AGE-RAGE) pathway-related genes CCL2 and interleukin-1β (IL-1β) play an important role in the biological of CBD. The expression of CCL2 and IL-1β were significantly increased in HMCs. Whereas, treatment with CBD decreased the expression of CCL2 and IL-1β. In addition, CBD significantly reduced AGE-RAGE levels in high glucose-induced HMCs. Similar results were confirmed in diabetic mice. In conclusion, we discovered for the first time that CBD ameliorates hyperglycemia partly through AGE-RAGE mediated CCL2/IL-1β pathway.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37486107</pmid><doi>10.1002/ddr.22093</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-1977-1035</orcidid></addata></record> |
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| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Advanced glycosylation end products Age Cannabidiol Cannabinoids Cannabis Cluster analysis Comorbidity Diabetes Diabetes mellitus Drug therapy Genes Glucose Glycosylation Hyperglycemia Hypoglycemia Inflammation Inflammatory response Mesangial cells Monocyte chemoattractant protein 1 |
| title | Cannabidiol ameliorates inflammatory response partly by AGE-RAGE pathway in diabetic mice |
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