Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway
The pathological damage of mesangial cells serves an important role in the occurrence and development of diabetic nephropathy. Ellagic acidhas beenreported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nep...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2021-09, Vol.22 (3), Article 1017 |
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| creator | Lin, Wei Liu, Guojian Kang, Xiaowen Guo, Ping Shang, Yu Du, Ruomei Wang, Xiyue Chen, Liting Yue, Rui Kong, Fanwu Zhu, Qihan |
| description | The pathological damage of mesangial cells serves an important role in the occurrence and development of diabetic nephropathy. Ellagic acidhas beenreported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nephropathy are unclear. The main aim of the present study was to investigate the effect of ellagic acid on high glucose-induced mesangial cell damage. The results revealed that high glucose could induce the hyperproliferation of mesangial cells, decrease the activity of superoxide dismutase, increase the malondialdehyde content, the level of reactive oxygen species, the secretion of inflammatory factors (TNF-[alpha], IL-1[beta] and IL-6) and the synthesis of extracellular matrix (Fibronectin, MMP-9 and TIMP-1) and activate the PI3K/Akt/FOXO3a signaling pathway. Ellagic acid could attenuate the injury of mesangial cells induced by high glucose in a concentration-dependent manner and its effect was consistent with that of a PI3K inhibitor (LY294002). Moreover, a PI3K agonist (740Y-P) reversed the protective effect of ellagic acid on mesangial cells induced by high glucose. In conclusion, ellagic acid protected mesangial cells from high glucose-induced injury in a concentration-dependent manner. The mechanism may be associated with ellagic acid inhibiting the activation of the PI3K/Akt signaling pathway and reducing the expression levels of downstream transcription factor FOXO3a. Key words: ellagic acid, mesangial cells, diabetic nephropathy, PI3K/Akt, FOXO3a |
| doi_str_mv | 10.3892/etm.2021.10449 |
| format | Article |
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Ellagic acidhas beenreported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nephropathy are unclear. The main aim of the present study was to investigate the effect of ellagic acid on high glucose-induced mesangial cell damage. The results revealed that high glucose could induce the hyperproliferation of mesangial cells, decrease the activity of superoxide dismutase, increase the malondialdehyde content, the level of reactive oxygen species, the secretion of inflammatory factors (TNF-[alpha], IL-1[beta] and IL-6) and the synthesis of extracellular matrix (Fibronectin, MMP-9 and TIMP-1) and activate the PI3K/Akt/FOXO3a signaling pathway. Ellagic acid could attenuate the injury of mesangial cells induced by high glucose in a concentration-dependent manner and its effect was consistent with that of a PI3K inhibitor (LY294002). Moreover, a PI3K agonist (740Y-P) reversed the protective effect of ellagic acid on mesangial cells induced by high glucose. In conclusion, ellagic acid protected mesangial cells from high glucose-induced injury in a concentration-dependent manner. The mechanism may be associated with ellagic acid inhibiting the activation of the PI3K/Akt signaling pathway and reducing the expression levels of downstream transcription factor FOXO3a. Key words: ellagic acid, mesangial cells, diabetic nephropathy, PI3K/Akt, FOXO3a</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2021.10449</identifier><identifier>PMID: 34373703</identifier><language>eng</language><publisher>Athens: Spandidos Publications</publisher><subject>Alzheimer's disease ; Biotechnology ; Care and treatment ; Cell culture ; Cellular signal transduction ; Connective tissue cells ; Diabetes ; Diabetic nephropathies ; Diabetic nephropathy ; Ellagic acid ; Genetic aspects ; Glucose ; Health aspects ; Kidney glomerulus ; Oxidative stress ; Protein kinases ; Proteins ; Reactive oxygen species ; Transcription factors</subject><ispartof>Experimental and therapeutic medicine, 2021-09, Vol.22 (3), Article 1017</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Lin et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-f99262930a1183c43e4b134169832bde3f01e9f7c6f13aee498811684270951e3</citedby><cites>FETCH-LOGICAL-c392t-f99262930a1183c43e4b134169832bde3f01e9f7c6f13aee498811684270951e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8343806/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8343806/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Lin, Wei</creatorcontrib><creatorcontrib>Liu, Guojian</creatorcontrib><creatorcontrib>Kang, Xiaowen</creatorcontrib><creatorcontrib>Guo, Ping</creatorcontrib><creatorcontrib>Shang, Yu</creatorcontrib><creatorcontrib>Du, Ruomei</creatorcontrib><creatorcontrib>Wang, Xiyue</creatorcontrib><creatorcontrib>Chen, Liting</creatorcontrib><creatorcontrib>Yue, Rui</creatorcontrib><creatorcontrib>Kong, Fanwu</creatorcontrib><creatorcontrib>Zhu, Qihan</creatorcontrib><title>Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway</title><title>Experimental and therapeutic medicine</title><description>The pathological damage of mesangial cells serves an important role in the occurrence and development of diabetic nephropathy. Ellagic acidhas beenreported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nephropathy are unclear. The main aim of the present study was to investigate the effect of ellagic acid on high glucose-induced mesangial cell damage. The results revealed that high glucose could induce the hyperproliferation of mesangial cells, decrease the activity of superoxide dismutase, increase the malondialdehyde content, the level of reactive oxygen species, the secretion of inflammatory factors (TNF-[alpha], IL-1[beta] and IL-6) and the synthesis of extracellular matrix (Fibronectin, MMP-9 and TIMP-1) and activate the PI3K/Akt/FOXO3a signaling pathway. Ellagic acid could attenuate the injury of mesangial cells induced by high glucose in a concentration-dependent manner and its effect was consistent with that of a PI3K inhibitor (LY294002). Moreover, a PI3K agonist (740Y-P) reversed the protective effect of ellagic acid on mesangial cells induced by high glucose. In conclusion, ellagic acid protected mesangial cells from high glucose-induced injury in a concentration-dependent manner. The mechanism may be associated with ellagic acid inhibiting the activation of the PI3K/Akt signaling pathway and reducing the expression levels of downstream transcription factor FOXO3a. Key words: ellagic acid, mesangial cells, diabetic nephropathy, PI3K/Akt, FOXO3a</description><subject>Alzheimer's disease</subject><subject>Biotechnology</subject><subject>Care and treatment</subject><subject>Cell culture</subject><subject>Cellular signal transduction</subject><subject>Connective tissue cells</subject><subject>Diabetes</subject><subject>Diabetic nephropathies</subject><subject>Diabetic nephropathy</subject><subject>Ellagic acid</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Health aspects</subject><subject>Kidney glomerulus</subject><subject>Oxidative stress</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Transcription factors</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkcFu1DAQhiMEolXplbMlzrvr8TiJfUFaVS1UVNoeQOJmeZ1J4sVJlthptTdegVfkScjSFQip48NY_sefZubPsrfAl6i0WFHqloILWAKXUr_IzqHUYgEc8penO9cKzrLLGHd8jrwApfLX2RlKLLHkeJ6l6xBs4x2zzlfM963f-hRZ65uWNWFyQ6RfP376vpocHfXdNB7mxEabWEfR9o23gTkKIbIHb1lqid3f4qfV-lta3Wy-btCy6JveBt83bG9T-2gPb7JXtQ2RLk_5Ivtyc_356uPibvPh9mp9t3CoRVrUWotCaOQWQKGTSHILKKHQCsW2Iqw5kK5LV9SAlkhqpQAKJUXJdQ6EF9n7J-5-2nZUOerTaIPZj76z48EM1pv_ld63phkejJoXpHgxA96dAOPwfaKYzG6YxnmYaERe8LyEEvm_qsYGMr6vhxnmOh-dWRclyhKkPrKWz1TNp6LOu6Gn2s_vz31w4xDjSPXfxoGbo_9m9t8c_Td__Mffxjqg1g</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Lin, Wei</creator><creator>Liu, Guojian</creator><creator>Kang, Xiaowen</creator><creator>Guo, Ping</creator><creator>Shang, Yu</creator><creator>Du, Ruomei</creator><creator>Wang, Xiyue</creator><creator>Chen, Liting</creator><creator>Yue, Rui</creator><creator>Kong, Fanwu</creator><creator>Zhu, Qihan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Ellagic acidhas beenreported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nephropathy are unclear. The main aim of the present study was to investigate the effect of ellagic acid on high glucose-induced mesangial cell damage. The results revealed that high glucose could induce the hyperproliferation of mesangial cells, decrease the activity of superoxide dismutase, increase the malondialdehyde content, the level of reactive oxygen species, the secretion of inflammatory factors (TNF-[alpha], IL-1[beta] and IL-6) and the synthesis of extracellular matrix (Fibronectin, MMP-9 and TIMP-1) and activate the PI3K/Akt/FOXO3a signaling pathway. Ellagic acid could attenuate the injury of mesangial cells induced by high glucose in a concentration-dependent manner and its effect was consistent with that of a PI3K inhibitor (LY294002). Moreover, a PI3K agonist (740Y-P) reversed the protective effect of ellagic acid on mesangial cells induced by high glucose. In conclusion, ellagic acid protected mesangial cells from high glucose-induced injury in a concentration-dependent manner. The mechanism may be associated with ellagic acid inhibiting the activation of the PI3K/Akt signaling pathway and reducing the expression levels of downstream transcription factor FOXO3a. Key words: ellagic acid, mesangial cells, diabetic nephropathy, PI3K/Akt, FOXO3a</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><pmid>34373703</pmid><doi>10.3892/etm.2021.10449</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer's disease Biotechnology Care and treatment Cell culture Cellular signal transduction Connective tissue cells Diabetes Diabetic nephropathies Diabetic nephropathy Ellagic acid Genetic aspects Glucose Health aspects Kidney glomerulus Oxidative stress Protein kinases Proteins Reactive oxygen species Transcription factors |
| title | Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway |
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