The protective role of corilagin on renal calcium oxalate crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt pathway in rats

Kidney stones, also known as calcium oxalate (CaOx) nephrolithiasis, are often asymptomatic, leading to kidney injury and renal failure complications. Corilagin is a gallotannin found in various plants and is known to elicit various biological activities. The present study aimed to elucidate the ren...

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Veröffentlicht in:Biotechnology and applied biochemistry 2021-12, Vol.68 (6), p.1323-1331, Article bab.2054
Hauptverfasser: Yuan, Haibo, Zhang, Jinghong, Yin, Xiaosong, Liu, Tongwei, Yue, Xiao, Li, Chuangui, Wang, Yuanyuan, Li, Ding, Wang, Qiang
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container_issue 6
container_start_page 1323
container_title Biotechnology and applied biochemistry
container_volume 68
creator Yuan, Haibo
Zhang, Jinghong
Yin, Xiaosong
Liu, Tongwei
Yue, Xiao
Li, Chuangui
Wang, Yuanyuan
Li, Ding
Wang, Qiang
description Kidney stones, also known as calcium oxalate (CaOx) nephrolithiasis, are often asymptomatic, leading to kidney injury and renal failure complications. Corilagin is a gallotannin found in various plants and is known to elicit various biological activities. The present study aimed to elucidate the renoprotective effect of corilagin against the rats’ renal stones deposition. The rats were induced for nephrolithiasis (CaOx deposition) using 0.75% ethylene glycol in their drinking water. Then, they were treated with corilagin at 50 and 100 mg/kg/day for 4 weeks. At the end of the experimental period, the rats were killed; blood and renal tissues were collected for various histological, biochemical, and gene expression analyses. The results demonstrated that the rats had renal calculi displaying a significant increase in serum creatinine (59.39 μmol/L) and blood urea nitrogen (19.03 mmol/L) levels compared with controls. Moreover, the malondialdehyde (13.29 nmol/mg) level was found to increase with a profound reduction in antioxidants’ activities with upregulated inflammatory cytokines. In contrast, the RT‐PCR and immunohistochemistry analysis demonstrated a substantial reduction in cell survival markers PPAR‐γ and PI3K/Akt with an apparent increase in apoptosis markers genes expressions in rats suffering from renal stones. Thus, the present study results suggest that corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt‐mediated pathway. Corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt mediated pathway
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Corilagin is a gallotannin found in various plants and is known to elicit various biological activities. The present study aimed to elucidate the renoprotective effect of corilagin against the rats’ renal stones deposition. The rats were induced for nephrolithiasis (CaOx deposition) using 0.75% ethylene glycol in their drinking water. Then, they were treated with corilagin at 50 and 100 mg/kg/day for 4 weeks. At the end of the experimental period, the rats were killed; blood and renal tissues were collected for various histological, biochemical, and gene expression analyses. The results demonstrated that the rats had renal calculi displaying a significant increase in serum creatinine (59.39 μmol/L) and blood urea nitrogen (19.03 mmol/L) levels compared with controls. Moreover, the malondialdehyde (13.29 nmol/mg) level was found to increase with a profound reduction in antioxidants’ activities with upregulated inflammatory cytokines. In contrast, the RT‐PCR and immunohistochemistry analysis demonstrated a substantial reduction in cell survival markers PPAR‐γ and PI3K/Akt with an apparent increase in apoptosis markers genes expressions in rats suffering from renal stones. Thus, the present study results suggest that corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt‐mediated pathway. Corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt mediated pathway</description><identifier>ISSN: 0885-4513</identifier><identifier>EISSN: 1470-8744</identifier><identifier>DOI: 10.1002/bab.2054</identifier><identifier>PMID: 33080078</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Antioxidants ; Apoptosis ; Apoptosis - drug effects ; Biomarkers ; Blood ; Calcium ; Calcium oxalate ; Calcium Oxalate - antagonists &amp; inhibitors ; Calcium Oxalate - pharmacology ; Calculi ; Cell survival ; Complications ; corilagin ; Creatinine ; Crystallization ; Cytokines ; Deposition ; Drinking water ; Ethylene glycol ; Gallotannin ; Gene expression ; Glucosides - pharmacology ; Hydrolyzable Tannins - pharmacology ; Immunohistochemistry ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Inflammatory response ; Kidney stones ; Kidneys ; Male ; Malondialdehyde ; Nephrolithiasis ; Oxalic acid ; Oxidative stress ; Oxidative Stress - drug effects ; Peroxisome proliferator-activated receptors ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K/Akt pathway ; PPAR gamma - antagonists &amp; inhibitors ; PPAR gamma - metabolism ; Protective Agents - pharmacology ; Proto-Oncogene Proteins c-akt - antagonists &amp; inhibitors ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Reduction ; Renal failure ; Signal Transduction - drug effects ; Urea</subject><ispartof>Biotechnology and applied biochemistry, 2021-12, Vol.68 (6), p.1323-1331, Article bab.2054</ispartof><rights>2020 International Union of Biochemistry and Molecular Biology, Inc.</rights><rights>2021 International Union of Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3494-6ead7ff146eb27eb0fa23d7f6a7db07aacbf45dee8e908b3c34ee1405cd9e64a3</citedby><cites>FETCH-LOGICAL-c3494-6ead7ff146eb27eb0fa23d7f6a7db07aacbf45dee8e908b3c34ee1405cd9e64a3</cites><orcidid>0000-0002-2731-1584 ; 0000-0002-6644-8276</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fbab.2054$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fbab.2054$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33080078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Haibo</creatorcontrib><creatorcontrib>Zhang, Jinghong</creatorcontrib><creatorcontrib>Yin, Xiaosong</creatorcontrib><creatorcontrib>Liu, Tongwei</creatorcontrib><creatorcontrib>Yue, Xiao</creatorcontrib><creatorcontrib>Li, Chuangui</creatorcontrib><creatorcontrib>Wang, Yuanyuan</creatorcontrib><creatorcontrib>Li, Ding</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><title>The protective role of corilagin on renal calcium oxalate crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt pathway in rats</title><title>Biotechnology and applied biochemistry</title><addtitle>Biotechnol Appl Biochem</addtitle><description>Kidney stones, also known as calcium oxalate (CaOx) nephrolithiasis, are often asymptomatic, leading to kidney injury and renal failure complications. Corilagin is a gallotannin found in various plants and is known to elicit various biological activities. The present study aimed to elucidate the renoprotective effect of corilagin against the rats’ renal stones deposition. The rats were induced for nephrolithiasis (CaOx deposition) using 0.75% ethylene glycol in their drinking water. Then, they were treated with corilagin at 50 and 100 mg/kg/day for 4 weeks. At the end of the experimental period, the rats were killed; blood and renal tissues were collected for various histological, biochemical, and gene expression analyses. The results demonstrated that the rats had renal calculi displaying a significant increase in serum creatinine (59.39 μmol/L) and blood urea nitrogen (19.03 mmol/L) levels compared with controls. Moreover, the malondialdehyde (13.29 nmol/mg) level was found to increase with a profound reduction in antioxidants’ activities with upregulated inflammatory cytokines. In contrast, the RT‐PCR and immunohistochemistry analysis demonstrated a substantial reduction in cell survival markers PPAR‐γ and PI3K/Akt with an apparent increase in apoptosis markers genes expressions in rats suffering from renal stones. Thus, the present study results suggest that corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt‐mediated pathway. Corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt mediated pathway</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biomarkers</subject><subject>Blood</subject><subject>Calcium</subject><subject>Calcium oxalate</subject><subject>Calcium Oxalate - antagonists &amp; inhibitors</subject><subject>Calcium Oxalate - pharmacology</subject><subject>Calculi</subject><subject>Cell survival</subject><subject>Complications</subject><subject>corilagin</subject><subject>Creatinine</subject><subject>Crystallization</subject><subject>Cytokines</subject><subject>Deposition</subject><subject>Drinking water</subject><subject>Ethylene glycol</subject><subject>Gallotannin</subject><subject>Gene expression</subject><subject>Glucosides - pharmacology</subject><subject>Hydrolyzable Tannins - pharmacology</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Kidney stones</subject><subject>Kidneys</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Nephrolithiasis</subject><subject>Oxalic acid</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K/Akt pathway</subject><subject>PPAR gamma - antagonists &amp; inhibitors</subject><subject>PPAR gamma - metabolism</subject><subject>Protective Agents - pharmacology</subject><subject>Proto-Oncogene Proteins c-akt - antagonists &amp; inhibitors</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reduction</subject><subject>Renal failure</subject><subject>Signal Transduction - drug effects</subject><subject>Urea</subject><issn>0885-4513</issn><issn>1470-8744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9u1TAQhy0Eoo-CxAmQJTZdNK0dO4mzfK34U1GJJ1TW0cSZUBcnDrbTkh1H4CKsuAeH4CT4vRaQkFiNNPPNt_j9CHnK2RFnLD9uoT3KWSHvkRWXFctUJeV9smJKFZksuNgjj0K4YoypSuUPyZ4QTDFWqRX5dnGJdPIuoo7mGql3FqnrqXbeWPhgRupG6nEESzVYbeaBus9gISLVfgkR7M8vX83YzRq7dDEd7DQhegzhkJqxtzAMEJ1fkiZMbgx4SGHsKExuii6YQK8N0M1m_S6Zfnzf3TZn4s3x-mOkE8TLG1iSh3qI4TF50IMN-ORu7pP3L19cnL7Ozt--Ojtdn2dayFpmJUJX9T2XJbZ5hS3rIRdpU0LVtawC0G0viw5RYc1UK9IXIpes0F2NpQSxTw5uvSmZTzOG2AwmaLQWRnRzaHJZ5LXioqwT-vwf9MrNPuWVqJJvIy9E_VeovQvBY99M3gzgl4azZlthkypsthUm9NmdcG4H7P6AvztLQHYL3BiLy39Fzcn6ZCf8BfEdqrM</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Yuan, Haibo</creator><creator>Zhang, Jinghong</creator><creator>Yin, Xiaosong</creator><creator>Liu, Tongwei</creator><creator>Yue, Xiao</creator><creator>Li, Chuangui</creator><creator>Wang, Yuanyuan</creator><creator>Li, Ding</creator><creator>Wang, Qiang</creator><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TB</scope><scope>7TK</scope><scope>7U5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>L7M</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2731-1584</orcidid><orcidid>https://orcid.org/0000-0002-6644-8276</orcidid></search><sort><creationdate>202112</creationdate><title>The protective role of corilagin on renal calcium oxalate crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt pathway in rats</title><author>Yuan, Haibo ; 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Corilagin is a gallotannin found in various plants and is known to elicit various biological activities. The present study aimed to elucidate the renoprotective effect of corilagin against the rats’ renal stones deposition. The rats were induced for nephrolithiasis (CaOx deposition) using 0.75% ethylene glycol in their drinking water. Then, they were treated with corilagin at 50 and 100 mg/kg/day for 4 weeks. At the end of the experimental period, the rats were killed; blood and renal tissues were collected for various histological, biochemical, and gene expression analyses. The results demonstrated that the rats had renal calculi displaying a significant increase in serum creatinine (59.39 μmol/L) and blood urea nitrogen (19.03 mmol/L) levels compared with controls. Moreover, the malondialdehyde (13.29 nmol/mg) level was found to increase with a profound reduction in antioxidants’ activities with upregulated inflammatory cytokines. In contrast, the RT‐PCR and immunohistochemistry analysis demonstrated a substantial reduction in cell survival markers PPAR‐γ and PI3K/Akt with an apparent increase in apoptosis markers genes expressions in rats suffering from renal stones. Thus, the present study results suggest that corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt‐mediated pathway. Corilagin could suppress renal CaOx crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt mediated pathway</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33080078</pmid><doi>10.1002/bab.2054</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2731-1584</orcidid><orcidid>https://orcid.org/0000-0002-6644-8276</orcidid></addata></record>
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subjects 1-Phosphatidylinositol 3-kinase
AKT protein
Animals
Antioxidants
Apoptosis
Apoptosis - drug effects
Biomarkers
Blood
Calcium
Calcium oxalate
Calcium Oxalate - antagonists & inhibitors
Calcium Oxalate - pharmacology
Calculi
Cell survival
Complications
corilagin
Creatinine
Crystallization
Cytokines
Deposition
Drinking water
Ethylene glycol
Gallotannin
Gene expression
Glucosides - pharmacology
Hydrolyzable Tannins - pharmacology
Immunohistochemistry
Inflammation
Inflammation - drug therapy
Inflammation - metabolism
Inflammatory response
Kidney stones
Kidneys
Male
Malondialdehyde
Nephrolithiasis
Oxalic acid
Oxidative stress
Oxidative Stress - drug effects
Peroxisome proliferator-activated receptors
Phosphatidylinositol 3-Kinases - metabolism
PI3K/Akt pathway
PPAR gamma - antagonists & inhibitors
PPAR gamma - metabolism
Protective Agents - pharmacology
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Wistar
Reduction
Renal failure
Signal Transduction - drug effects
Urea
title The protective role of corilagin on renal calcium oxalate crystal‐induced oxidative stress, inflammatory response, and apoptosis via PPAR‐γ and PI3K/Akt pathway in rats
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