Elucidating the Molecular Mechanism by Which Gallic Acid Alleviates Oxidative Stress and Inflammatory Response of Acrylamide-Induced Renal Injury in a Rat Model

Samet Tekin

Article Details

Elucidating the Molecular Mechanism by Which Gallic Acid Alleviates Oxidative Stress and Inflammatory Response of Acrylamide-Induced Renal Injury in a Rat Model

Authors:

Samet Tekin

Publisher:

Ataturk University

Main Topics:

Veteriner Anatomi ve Fizyoloji

Journal:

Veterinary Sciences and Practices Vol.19 Issue 2, pp.78-84

Document Type:

Article

Publication Date:

8/2024

Document Language:

English

Document ID (Org No.):

2001325992

pISSN:

2822-3608

Keywords:

Abstract:

 This study investigates the molecular effects of Acrylamide ACR-induced kidney damage and the potential protective role of Gallic acid GA. Forty male rats were divided into five groups: Control, ACR, ACRGA50, ACRGA100, and GA100. The ACR groups received a daily oral dose of 50 mgkg, while GA groups received 50 or 100 mgkg oral doses for 14 consecutive days. On the 15th day, the animals were euthanized, and kidney samples were collected. The MDA, GSH, SOD, GPx, and CAT oxidative stress parameters were measured. The renal inflammatory response was evaluated by measuring the level of TNF-α, IL-1β, IL-6, NF-κB, COX-2, and IL-10. The downstream pro-apoptotic signaling pathway was resolved by measuring the levels of p38 MAPK and p53. The ACR induced renal oxidative stress with aggravated lipid peroxidation as revealed by the reduction in the levels GSH, SOD, GPx, and CAT of antioxidants while over-increase in the level of MDA, respectively. The levels of IL-1β, IL-6, NF-kB, COX-2 pro-inflammatory mediators as well as the p38 MAPK and p53 pro-apoptotic intermediates were further elevated. This increase in inflammatory response was met with marked decrease in anti-inflammatory IL-10 level. However, GA treatments- in dose dependent manner- had been demonstrated to effectively mitigate oxidative stress and reduce inflammatory responses, while also enhancing the cellular anti-inflammatory defense mechanisms. The GA can be considered as a novel protective antioxidant, anti-apoptotic drug against ACR-induced nephrotoxic insult. Further study should be performed to estimate the exact effective dose.

 This study investigates the molecular effects of Acrylamide ACR-induced kidney damage and the potential protective role of Gallic acid GA. Forty male rats were divided into five groups: Control, ACR, ACRGA50, ACRGA100, and GA100. The ACR groups received a daily oral dose of 50 mgkg, while GA groups received 50 or 100 mgkg oral doses for 14 consecutive days. On the 15th day, the animals were euthanized, and kidney samples were collected. The MDA, GSH, SOD, GPx, and CAT oxidative stress parameters were measured. The renal inflammatory response was evaluated by measuring the level of TNF-α, IL-1β, IL-6, NF-κB, COX-2, and IL-10. The downstream pro-apoptotic signaling pathway was resolved by measuring the levels of p38 MAPK and p53. The ACR induced renal oxidative stress with aggravated lipid peroxidation as revealed by the reduction in the levels GSH, SOD, GPx, and CAT of antioxidants while over-increase in the level of MDA, respectively. The levels of IL-1β, IL-6, NF-kB, COX-2 pro-inflammatory mediators as well as the p38 MAPK and p53 pro-apoptotic intermediates were further elevated. This increase in inflammatory response was met with marked decrease in anti-inflammatory IL-10 level. However, GA treatments- in dose dependent manner- had been demonstrated to effectively mitigate oxidative stress and reduce inflammatory responses, while also enhancing the cellular anti-inflammatory defense mechanisms. The GA can be considered as a novel protective antioxidant, anti-apoptotic drug against ACR-induced nephrotoxic insult. Further study should be performed to estimate the exact effective dose.

 This study investigates the molecular effects of Acrylamide ACR-induced kidney damage and the potential protective role of Gallic acid GA. Forty male rats were divided into five groups: Control, ACR, ACRGA50, ACRGA100, and GA100. The ACR groups received a daily oral dose of 50 mgkg, while GA groups received 50 or 100 mgkg oral doses for 14 consecutive days. On the 15th day, the animals were euthanized, and kidney samples were collected. The MDA, GSH, SOD, GPx, and CAT oxidative stress parameters were measured. The renal inflammatory response was evaluated by measuring the level of TNF-α, IL-1β, IL-6, NF-κB, COX-2, and IL-10. The downstream pro-apoptotic signaling pathway was resolved by measuring the levels of p38 MAPK and p53. The ACR induced renal oxidative stress with aggravated lipid peroxidation as revealed by the reduction in the levels GSH, SOD, GPx, and CAT of antioxidants while over-increase in the level of MDA, respectively. The levels of IL-1β, IL-6, NF-kB, COX-2 pro-inflammatory mediators as well as the p38 MAPK and p53 pro-apoptotic intermediates were further elevated. This increase in inflammatory response was met with marked decrease in anti-inflammatory IL-10 level. However, GA treatments- in dose dependent manner- had been demonstrated to effectively mitigate oxidative stress and reduce inflammatory responses, while also enhancing the cellular anti-inflammatory defense mechanisms. The GA can be considered as a novel protective antioxidant, anti-apoptotic drug against ACR-induced nephrotoxic insult. Further study should be performed to estimate the exact effective dose.

 Bu çalışma, Akrilamid ACR kaynaklı böbrek hasarının moleküler etkilerini ve Galik asidin GA potansiyel koruyucu rolünü araştırmaktadır. Kırk erkek sıçan, Kontrol, ACR, ACRGA50, ACRGA100 ve GA100 olmak üzere beş gruba ayrılmıştır. ACR grupları günlük oral 50 mgkg dozda alırken, GA grupları ise 14 ardışık gün boyunca 50 veya 100 mgkg oral dozda almıştır. 15. gününde hayvanlar uyuşturularak böbrek örnekleri alınmıştır. MDA, GSH, SOD, GPx ve CAT oksidatif stres parametreleri ölçülmüştür. Böbrek iltihabi yanıtı, TNF-α, IL-1β, IL-6, NF-κB, COX-2 ve IL-10 seviyeleri ölçülerek değerlendirilmiştir. Aşağı akım pro-apoptotik sinyal yolakları, p38 MAPK ve p53 seviyeleri ölçülerek çözümlenmiştir. ACR, antioksidanların GSH, SOD, GPx ve CAT seviyelerinde azalma ve MDA seviyesinde artış ile belirginleşen lipid peroksidasyonunu şiddetlendirerek renal oksidatif stresi tetiklemiştir. IL-1β, IL-6, NF-kB, COX-2 pro-iltihabi mediatörler ve ayrıca p38 MAPK ve p53 pro-apoptotik ara maddelerin seviyeleri artmıştır. Bu artan iltihabi yanıt, anti-iltihabi IL-10 seviyesinde belirgin bir azalma ile karşılanmıştır. Bununla birlikte, doza bağlı olarak GA tedavilerinin oksidatif stresi etkin bir şekilde azalttığı, iltihabi yanıtları düşürdüğü ve hücresel anti-iltihabi savunma mekanizmalarını artırdığı gösterilmiştir. GA, ACR kaynaklı böbrek hasarına karşı yeni bir koruyucu antioksidan ve anti-apoptotik ilaç olarak değerlendirilebilir. Kesin etkili dozu belirlemek için ileri çalışmalar yapılmalıdır.

Article Details

Elucidating the Molecular Mechanism by Which Gallic Acid Alleviates Oxidative Stress and Inflammatory Response of Acrylamide-Induced Renal Injury in a Rat Model

Authors:

Samet Tekin

Publisher:

Ataturk University

Main Topics:

Veteriner Anatomi ve Fizyoloji

Journal:

Veterinary Sciences and Practices Vol.19 Issue 2, pp.78-84

Document Type:

Article

Publication Date:

8/2024

Document Language:

English

Document ID (Org No.):

2001325992

pISSN:

2822-3608

Acrylamide

apoptosis

gallic acid

inflammation

nephrotoxicityAkrilamid

apoptoz

galik asit

iltihap

nefrotoksisite

Issues

Article Details

Authors: Samet Tekin

Publisher: Ataturk University

Main Topics: Veteriner Anatomi ve Fizyoloji

Journal: Veterinary Sciences and Practices Vol.19 Issue 2, pp.78-84

Document Type: Article

Publication Date: 8/2024

Document Language: English

Document ID (Org No.): 2001325992

pISSN: 2822-3608

Issues

Authors:

Samet Tekin

Publisher:

Ataturk University

Main Topics:

Veteriner Anatomi ve Fizyoloji

Journal:

Veterinary Sciences and Practices Vol.19 Issue 2, pp.78-84

Document Type:

Article

Publication Date:

8/2024

Document Language:

English

Document ID (Org No.):

2001325992

pISSN:

2822-3608