Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway

Chemicals can induce nephrotoxicity, with damage to different segments of the nephron and deterioration of renal function. Nephrotoxicity due to exposure to a toxin such as carbon tetrachloride, sodium oxalate, or heavy metals is the most common cause of kidney injury. The current study aimed to eva...

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Autores principales:	Karunakaran Balaji, Jagadish Vijayakumar, Ponnusamy Kasirajan Sankaran, Sivanesan Senthilkumar, Rajagopalan Vijayaraghavan, Jayaraman Selvaraj, Maria Francis Yuvaraj
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	<i>Celastrus paniculatus</i> nephroprotective electron microscopy lead acetate nephrotoxicity P13K/AKT signaling pathway Organic chemistry QD241-441
Acceso en línea:	https://doaj.org/article/9122322e17374a059180208f51a8aea9
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spelling	oai:doaj.org-article:9122322e17374a059180208f51a8aea92021-11-11T18:36:49ZMolecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway10.3390/molecules262166471420-3049https://doaj.org/article/9122322e17374a059180208f51a8aea92021-11-01T00:00:00Zhttps://www.mdpi.com/1420-3049/26/21/6647https://doaj.org/toc/1420-3049Chemicals can induce nephrotoxicity, with damage to different segments of the nephron and deterioration of renal function. Nephrotoxicity due to exposure to a toxin such as carbon tetrachloride, sodium oxalate, or heavy metals is the most common cause of kidney injury. The current study aimed to evaluate the protective effects of <i>Celastrus paniculatus</i> seed extract against lead-acetate-induced nephrotoxicity by evaluating the histopathology, immunohistochemistry, ultrastructure, and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Twenty-four rats were divided into four groups (<i>n</i> = 6 per group): group 1 contained normal animals and served as the control; group 2 received lead acetate (30 mg/kg body weight (b.w.)/day, oral); group 3 received lead acetate and the standard drug <i>N</i>-acetylcysteine (NAC, 200 mg/kg b.w./day, oral); and group 4 received lead acetate and the ethanolic extract of <i>C. paniculatus</i> seed (EECP; 800 mg/kg b.w./day, oral). Treatment was given for 28 consecutive days. The data were analyzed using one-way analysis of variance with SIGMA PLOT 13 using SYSTAT software followed by Newman–Keul’s test for comparison between the groups. EECP ameliorated the adverse changes caused by lead acetate. PI3K and AKT messenger RNA (mRNA) levels were diminished in lead-acetate-treated rats. Treatment with EECP inhibited the occurrence of shrunken cells, the atrophy of glomeruli, and degenerative changes in renal tubules caused by lead acetate. Interestingly, the PI3K and AKT mRNA levels were significantly increased in EECP-treated animals. Our results clearly evidence for the first time that <i>C. paniculatus</i> seed extract inhibits lead-acetate-induced detrimental changes in kidneys by regulating PI3K/AKT signaling pathways.Karunakaran BalajiJagadish VijayakumarPonnusamy Kasirajan SankaranSivanesan SenthilkumarRajagopalan VijayaraghavanJayaraman SelvarajMaria Francis YuvarajMDPI AGarticle<i>Celastrus paniculatus</i>nephroprotectiveelectron microscopylead acetatenephrotoxicityP13K/AKT signaling pathwayOrganic chemistryQD241-441ENMolecules, Vol 26, Iss 6647, p 6647 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	<i>Celastrus paniculatus</i> nephroprotective electron microscopy lead acetate nephrotoxicity P13K/AKT signaling pathway Organic chemistry QD241-441
spellingShingle	<i>Celastrus paniculatus</i> nephroprotective electron microscopy lead acetate nephrotoxicity P13K/AKT signaling pathway Organic chemistry QD241-441 Karunakaran Balaji Jagadish Vijayakumar Ponnusamy Kasirajan Sankaran Sivanesan Senthilkumar Rajagopalan Vijayaraghavan Jayaraman Selvaraj Maria Francis Yuvaraj Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
description	Chemicals can induce nephrotoxicity, with damage to different segments of the nephron and deterioration of renal function. Nephrotoxicity due to exposure to a toxin such as carbon tetrachloride, sodium oxalate, or heavy metals is the most common cause of kidney injury. The current study aimed to evaluate the protective effects of <i>Celastrus paniculatus</i> seed extract against lead-acetate-induced nephrotoxicity by evaluating the histopathology, immunohistochemistry, ultrastructure, and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Twenty-four rats were divided into four groups (<i>n</i> = 6 per group): group 1 contained normal animals and served as the control; group 2 received lead acetate (30 mg/kg body weight (b.w.)/day, oral); group 3 received lead acetate and the standard drug <i>N</i>-acetylcysteine (NAC, 200 mg/kg b.w./day, oral); and group 4 received lead acetate and the ethanolic extract of <i>C. paniculatus</i> seed (EECP; 800 mg/kg b.w./day, oral). Treatment was given for 28 consecutive days. The data were analyzed using one-way analysis of variance with SIGMA PLOT 13 using SYSTAT software followed by Newman–Keul’s test for comparison between the groups. EECP ameliorated the adverse changes caused by lead acetate. PI3K and AKT messenger RNA (mRNA) levels were diminished in lead-acetate-treated rats. Treatment with EECP inhibited the occurrence of shrunken cells, the atrophy of glomeruli, and degenerative changes in renal tubules caused by lead acetate. Interestingly, the PI3K and AKT mRNA levels were significantly increased in EECP-treated animals. Our results clearly evidence for the first time that <i>C. paniculatus</i> seed extract inhibits lead-acetate-induced detrimental changes in kidneys by regulating PI3K/AKT signaling pathways.
format	article
author	Karunakaran Balaji Jagadish Vijayakumar Ponnusamy Kasirajan Sankaran Sivanesan Senthilkumar Rajagopalan Vijayaraghavan Jayaraman Selvaraj Maria Francis Yuvaraj
author_facet	Karunakaran Balaji Jagadish Vijayakumar Ponnusamy Kasirajan Sankaran Sivanesan Senthilkumar Rajagopalan Vijayaraghavan Jayaraman Selvaraj Maria Francis Yuvaraj
author_sort	Karunakaran Balaji
title	Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
title_short	Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
title_full	Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
title_fullStr	Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
title_full_unstemmed	Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway
title_sort	molecular studies on the nephroprotective potential of <i>celastrus paniculatus</i> against lead-acetate-induced nephrotoxicity in experimental rats: role of the pi3k/akt signaling pathway
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/9122322e17374a059180208f51a8aea9
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Molecular Studies on the Nephroprotective Potential of <i>Celastrus paniculatus</i> against Lead-Acetate-Induced Nephrotoxicity in Experimental Rats: Role of the PI3K/AKT Signaling Pathway

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