Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats

The aim of the current study was to evaluate the protective effects and mechanisms of isoliquiritigenin (ISO) on acute renal injury. CCK-8 assays were applied to assess the effects of ISO at different doses (20, 40, and 80 μg/mL) on oxidative damage in human renal HK-2 cells incubated with high gluc...

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Autores principales:	Leiming Sun, Zheng Yang, Jiaying Zhang, Jie Wang
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	isoliquiritigenin diabetic nephropathy oxidative damage fibrosis tgf-β/smad signaling pathway Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/980eb883e6384058b018ed173c5166b1
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spelling	oai:doaj.org-article:980eb883e6384058b018ed173c5166b12021-12-01T14:41:00ZIsoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats2165-59792165-598710.1080/21655979.2021.2006978https://doaj.org/article/980eb883e6384058b018ed173c5166b12021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2006978https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987The aim of the current study was to evaluate the protective effects and mechanisms of isoliquiritigenin (ISO) on acute renal injury. CCK-8 assays were applied to assess the effects of ISO at different doses (20, 40, and 80 μg/mL) on oxidative damage in human renal HK-2 cells incubated with high glucose. After the diabetic nephropathy (DN) rat model was established, the model animals were randomly assigned to saline-treated control, three model groups received the 10, 20 and 40 mg/kg ISO, respectively, using the healthy Sprague-Dawley (SD) rats as normal control. The blood biochemical indexes, renal functions, oxidative stress, morphological changes, fibrosis- and JAK2/STAT3-related factors in DN model rats were all assessed. The cellular viability of the renal HK-2 cells with oxidative damages were all markedly ameliorated via the incubation of ISO between 10 and 80 μg/mL compared with negative control. In addition, the significantly down-regulated ROS content and up-regulated expression levels of GSH, SOD2, and GPX1 were all observed in ISO-treated groups. Long-term administration of ISO at different doses in DN rats effectively improved general diabetic characteristics and renal morphology. Furthermore, long-term administration of ISO could ameliorate excessive oxidation stress, down-regulate the expression levels of renal fibrosis- and inflammation-related factors, as well as inhibit the JAK2/STAT3 signaling pathway. In conclusion, ISO at all three dosages could efficiently improve the renal injury induced by STZ via ameliorating renal fibrosis, oxidative stress, and inhibiting JAK2/STAT3 signaling pathways in the DN rats.Leiming SunZheng YangJiaying ZhangJie WangTaylor & Francis Grouparticleisoliquiritigenindiabetic nephropathyoxidative damagefibrosistgf-β/smad signaling pathwayBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 11188-11200 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	isoliquiritigenin diabetic nephropathy oxidative damage fibrosis tgf-β/smad signaling pathway Biotechnology TP248.13-248.65
spellingShingle	isoliquiritigenin diabetic nephropathy oxidative damage fibrosis tgf-β/smad signaling pathway Biotechnology TP248.13-248.65 Leiming Sun Zheng Yang Jiaying Zhang Jie Wang Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
description	The aim of the current study was to evaluate the protective effects and mechanisms of isoliquiritigenin (ISO) on acute renal injury. CCK-8 assays were applied to assess the effects of ISO at different doses (20, 40, and 80 μg/mL) on oxidative damage in human renal HK-2 cells incubated with high glucose. After the diabetic nephropathy (DN) rat model was established, the model animals were randomly assigned to saline-treated control, three model groups received the 10, 20 and 40 mg/kg ISO, respectively, using the healthy Sprague-Dawley (SD) rats as normal control. The blood biochemical indexes, renal functions, oxidative stress, morphological changes, fibrosis- and JAK2/STAT3-related factors in DN model rats were all assessed. The cellular viability of the renal HK-2 cells with oxidative damages were all markedly ameliorated via the incubation of ISO between 10 and 80 μg/mL compared with negative control. In addition, the significantly down-regulated ROS content and up-regulated expression levels of GSH, SOD2, and GPX1 were all observed in ISO-treated groups. Long-term administration of ISO at different doses in DN rats effectively improved general diabetic characteristics and renal morphology. Furthermore, long-term administration of ISO could ameliorate excessive oxidation stress, down-regulate the expression levels of renal fibrosis- and inflammation-related factors, as well as inhibit the JAK2/STAT3 signaling pathway. In conclusion, ISO at all three dosages could efficiently improve the renal injury induced by STZ via ameliorating renal fibrosis, oxidative stress, and inhibiting JAK2/STAT3 signaling pathways in the DN rats.
format	article
author	Leiming Sun Zheng Yang Jiaying Zhang Jie Wang
author_facet	Leiming Sun Zheng Yang Jiaying Zhang Jie Wang
author_sort	Leiming Sun
title	Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
title_short	Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
title_full	Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
title_fullStr	Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
title_full_unstemmed	Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats
title_sort	isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and jak2/stat3 pathway in streptozotocin-induced diabetic rats
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/980eb883e6384058b018ed173c5166b1
work_keys_str_mv	AT leimingsun isoliquiritigeninattenuatesacuterenalinjurythroughsuppressingoxidativestressfibrosisandjak2stat3pathwayinstreptozotocininduceddiabeticrats AT zhengyang isoliquiritigeninattenuatesacuterenalinjurythroughsuppressingoxidativestressfibrosisandjak2stat3pathwayinstreptozotocininduceddiabeticrats AT jiayingzhang isoliquiritigeninattenuatesacuterenalinjurythroughsuppressingoxidativestressfibrosisandjak2stat3pathwayinstreptozotocininduceddiabeticrats AT jiewang isoliquiritigeninattenuatesacuterenalinjurythroughsuppressingoxidativestressfibrosisandjak2stat3pathwayinstreptozotocininduceddiabeticrats
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Isoliquiritigenin attenuates acute renal injury through suppressing oxidative stress, fibrosis and JAK2/STAT3 pathway in streptozotocin-induced diabetic rats

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