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Conference Paper: A SMALL MOLECULE FROM GANODERMA LUCIDUM PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY VIA SUPPRESSING NLRP3/CASPASE-1 RELATED PYROPTOSIS

TitleA SMALL MOLECULE FROM GANODERMA LUCIDUM PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY VIA SUPPRESSING NLRP3/CASPASE-1 RELATED PYROPTOSIS
Authors
Issue Date2020
PublisherElsevier Inc. The Journal's web site is located at http://www.journals.elsevier.com/kidney-international-reports/
Citation
ISN World Congress of Nephrology (WCN), Abu Dhabi, United Arab Emirates, 26-29 March 2020. Abstracts in Kidney International Reports, 2020, v. 5 n. 3, Suppl., p. S217, abstract no. SUN-030 How to Cite?
AbstractIntroduction: Ganoderma lucidum (Lingzhi) is the medicinal fungi traditionally used to promote health and longevity. Previous studies indicate the Ganoderma lucidum potentially boosts the immune system and suppresses the inflammation in vivo and in vitro. Pyroptosis is a highly inflammatory form of programmed cell death. The study aimed to screen molecules against cisplatin-induced kidney injury. Methods: Forty-two molecules were isolated from Ganoderma lucidum and tested by the cell viability assay for screening protective effects. The mouse tubular epithelial cells (mTECs) were pre-treated with small molecules (20-60 mM) for 6 hours, followed by adding cisplatin (25 mM) for 24-48 hours. The molecular mechanisms of attenuating the cisplatininduced kidney injury were further examined. Results: Among 42 molecules, cell viability tests showed that six molecules significantly attenuated cisplatin-induced cytotoxicity in mTECs (p<0.0001). Molecular docking predicted qNFLZ may interact with an upstream protein of the NFkB pathway. The real-time PCR analysis showed that qNFLZ significantly reduced IL-1b and MCP-1. The western-blot analysis indicated qNFLZ suppressed the phosphorylation of NFkB P65, and activation of NLRP3, caspase-1 and Gasdermin D. The findings suggested qNFLZ protects against cisplatin-induced kidney injury via suppressing NLRP3-caspase-1-Gasdermin D pathway. Conclusions: The study demonstrates qNFLZ is a potential molecule to protect against cisplatin-induced kidney injury clinically.
DescriptionCongress was cancelled due to COVID-19
Persistent Identifierhttp://hdl.handle.net/10722/287848
ISSN
2019 Impact Factor: 3.374

 

DC FieldValueLanguage
dc.contributor.authorXue, L-
dc.contributor.authorWu, W-
dc.contributor.authorYou, Y-
dc.contributor.authorChen, H-
dc.date.accessioned2020-10-05T12:04:08Z-
dc.date.available2020-10-05T12:04:08Z-
dc.date.issued2020-
dc.identifier.citationISN World Congress of Nephrology (WCN), Abu Dhabi, United Arab Emirates, 26-29 March 2020. Abstracts in Kidney International Reports, 2020, v. 5 n. 3, Suppl., p. S217, abstract no. SUN-030-
dc.identifier.issn2468-0249-
dc.identifier.urihttp://hdl.handle.net/10722/287848-
dc.descriptionCongress was cancelled due to COVID-19-
dc.description.abstractIntroduction: Ganoderma lucidum (Lingzhi) is the medicinal fungi traditionally used to promote health and longevity. Previous studies indicate the Ganoderma lucidum potentially boosts the immune system and suppresses the inflammation in vivo and in vitro. Pyroptosis is a highly inflammatory form of programmed cell death. The study aimed to screen molecules against cisplatin-induced kidney injury. Methods: Forty-two molecules were isolated from Ganoderma lucidum and tested by the cell viability assay for screening protective effects. The mouse tubular epithelial cells (mTECs) were pre-treated with small molecules (20-60 mM) for 6 hours, followed by adding cisplatin (25 mM) for 24-48 hours. The molecular mechanisms of attenuating the cisplatininduced kidney injury were further examined. Results: Among 42 molecules, cell viability tests showed that six molecules significantly attenuated cisplatin-induced cytotoxicity in mTECs (p<0.0001). Molecular docking predicted qNFLZ may interact with an upstream protein of the NFkB pathway. The real-time PCR analysis showed that qNFLZ significantly reduced IL-1b and MCP-1. The western-blot analysis indicated qNFLZ suppressed the phosphorylation of NFkB P65, and activation of NLRP3, caspase-1 and Gasdermin D. The findings suggested qNFLZ protects against cisplatin-induced kidney injury via suppressing NLRP3-caspase-1-Gasdermin D pathway. Conclusions: The study demonstrates qNFLZ is a potential molecule to protect against cisplatin-induced kidney injury clinically.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.journals.elsevier.com/kidney-international-reports/-
dc.relation.ispartofKidney International Reports-
dc.relation.ispartofWorld Congress of Nephrology (WCN), 2020-
dc.titleA SMALL MOLECULE FROM GANODERMA LUCIDUM PROTECTS AGAINST CISPLATIN-INDUCED KIDNEY INJURY VIA SUPPRESSING NLRP3/CASPASE-1 RELATED PYROPTOSIS-
dc.typeConference_Paper-
dc.identifier.emailChen, H: haiyong@hku.hk-
dc.identifier.authorityChen, H=rp01923-
dc.description.natureabstract-
dc.identifier.doi10.1016/j.ekir.2020.02.553-
dc.identifier.hkuros314672-
dc.identifier.volume5-
dc.identifier.issue3, Suppl.-
dc.identifier.spageS217-
dc.identifier.epageS217-
dc.publisher.placeUnited States-
dc.identifier.issnl2468-0249-

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