Naringin protects against colistin-induced sciatic nerve damage by reducing oxidative stress, apoptosis and inflammation damage

Selçuk Yılmaz; Sefa Küçükler; Hasan Şimşek; Serpil Aygörmez; Fatih Mehmet Kandemir

Makale detayları

Naringin protects against colistin-induced sciatic nerve damage by reducing oxidative stress, apoptosis and inflammation damage

Yazarlar:

Selçuk Yılmaz | Sefa Küçükler | Hasan Şimşek | Serpil Aygörmez | Fatih Mehmet Kandemir

Yayıncı:

Ondokuz Mayıs University

Ana Başlıklar:

Orthopaedics

Dergi:

Deneysel ve Klinik Tıp Dergisi Vol.41 Issue 1, pp.53-59

Belge Tipi:

Makale

Yayın Tarihi:

3/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001314469

pISSN:

1309-4483

Anahtar kelimeler:

Özet:

 Colistin is used in treatment against gram-negative bacteria. It causes toxic effects due to oxidative stress in a dose-dependent manner. Naringin is a flavonoid with strong antioxidant properties found naturally in many plants, especially citrus fruits. This study aimed to determine the protective effects of NRG in CLS-induced sciatic nerve injury. Thirty-five male Spraque rats were randomly divided into five groups: control, NRG, CLS, CLSNRG50, and CLSNRG100. CLS was administered orally at a 15 mgkg dose for seven days. NRG was administered orally at 50 or 100 mgkg doses for seven days. Sciatic nerve tissues were collected and analyzed for oxidative stress markers, inflammation, and apoptosis damage levels by biochemical methods. CLS caused toxic damage in sciatic nerve tissue by increasing lipid peroxidation MDA and decreasing antioxidant capacity SOD, CAT, GPx, and GSH; increasing NF-κB, TNF-α, nNOS release; increasing apoptotic factor Caspase-3; decreasing HO-1 and nCAM; and inducing 8-OHdG, MAPK and GFAP p0.05. NRG, on the other hand, reversed all these changes in sciatic nerve tissue and reduced CLS-induced oxidative stress damage, inflammatory damage and apoptotic damage p0.05. These effects were more effective at the 100 mgkg dose of NRG than at the 50 mgkg dose p0.05. In sciatic nerve tissue, CLS induced sciatic nerve toxicity with increased oxidative stress, inflammation, and apoptotic damage. NRG showed a protective effect against CLS-induced sciatic nerve toxicity.

 Colistin is used in treatment against gram-negative bacteria. It causes toxic effects due to oxidative stress in a dose-dependent manner. Naringin is a flavonoid with strong antioxidant properties found naturally in many plants, especially citrus fruits. This study aimed to determine the protective effects of NRG in CLS-induced sciatic nerve injury. Thirty-five male Spraque rats were randomly divided into five groups: control, NRG, CLS, CLSNRG50, and CLSNRG100. CLS was administered orally at a 15 mgkg dose for seven days. NRG was administered orally at 50 or 100 mgkg doses for seven days. Sciatic nerve tissues were collected and analyzed for oxidative stress markers, inflammation, and apoptosis damage levels by biochemical methods. CLS caused toxic damage in sciatic nerve tissue by increasing lipid peroxidation MDA and decreasing antioxidant capacity SOD, CAT, GPx, and GSH; increasing NF-κB, TNF-α, nNOS release; increasing apoptotic factor Caspase-3; decreasing HO-1 and nCAM; and inducing 8-OHdG, MAPK and GFAP p0.05. NRG, on the other hand, reversed all these changes in sciatic nerve tissue and reduced CLS-induced oxidative stress damage, inflammatory damage and apoptotic damage p0.05. These effects were more effective at the 100 mgkg dose of NRG than at the 50 mgkg dose p0.05. In sciatic nerve tissue, CLS induced sciatic nerve toxicity with increased oxidative stress, inflammation, and apoptotic damage. NRG showed a protective effect against CLS-induced sciatic nerve toxicity.

 Colistin is used in treatment against gram-negative bacteria. It causes toxic effects due to oxidative stress in a dose-dependent manner. Naringin is a flavonoid with strong antioxidant properties found naturally in many plants, especially citrus fruits. This study aimed to determine the protective effects of NRG in CLS-induced sciatic nerve injury. Thirty-five male Spraque rats were randomly divided into five groups: control, NRG, CLS, CLSNRG50, and CLSNRG100. CLS was administered orally at a 15 mgkg dose for seven days. NRG was administered orally at 50 or 100 mgkg doses for seven days. Sciatic nerve tissues were collected and analyzed for oxidative stress markers, inflammation, and apoptosis damage levels by biochemical methods. CLS caused toxic damage in sciatic nerve tissue by increasing lipid peroxidation MDA and decreasing antioxidant capacity SOD, CAT, GPx, and GSH; increasing NF-κB, TNF-α, nNOS release; increasing apoptotic factor Caspase-3; decreasing HO-1 and nCAM; and inducing 8-OHdG, MAPK and GFAP p0.05. NRG, on the other hand, reversed all these changes in sciatic nerve tissue and reduced CLS-induced oxidative stress damage, inflammatory damage and apoptotic damage p0.05. These effects were more effective at the 100 mgkg dose of NRG than at the 50 mgkg dose p0.05. In sciatic nerve tissue, CLS induced sciatic nerve toxicity with increased oxidative stress, inflammation, and apoptotic damage. NRG showed a protective effect against CLS-induced sciatic nerve toxicity.

 Colistin is used in treatment against gram-negative bacteria. It causes toxic effects due to oxidative stress in a dose-dependent manner. Naringin is a flavonoid with strong antioxidant properties found naturally in many plants, especially citrus fruits. This study aimed to determine the protective effects of NRG in CLS-induced sciatic nerve injury. Thirty-five male Spraque rats were randomly divided into five groups: control, NRG, CLS, CLSNRG50, and CLSNRG100. CLS was administered orally at a 15 mgkg dose for seven days. NRG was administered orally at 50 or 100 mgkg doses for seven days. Sciatic nerve tissues were collected and analyzed for oxidative stress markers, inflammation, and apoptosis damage levels by biochemical methods. CLS caused toxic damage in sciatic nerve tissue by increasing lipid peroxidation MDA and decreasing antioxidant capacity SOD, CAT, GPx, and GSH; increasing NF-κB, TNF-α, nNOS release; increasing apoptotic factor Caspase-3; decreasing HO-1 and nCAM; and inducing 8-OHdG, MAPK and GFAP p0.05. NRG, on the other hand, reversed all these changes in sciatic nerve tissue and reduced CLS-induced oxidative stress damage, inflammatory damage and apoptotic damage p0.05. These effects were more effective at the 100 mgkg dose of NRG than at the 50 mgkg dose p0.05. In sciatic nerve tissue, CLS induced sciatic nerve toxicity with increased oxidative stress, inflammation, and apoptotic damage. NRG showed a protective effect against CLS-induced sciatic nerve toxicity.

Makale detayları

Naringin protects against colistin-induced sciatic nerve damage by reducing oxidative stress, apoptosis and inflammation damage

Yazarlar:

Selçuk Yılmaz | Sefa Küçükler | Hasan Şimşek | Serpil Aygörmez | Fatih Mehmet Kandemir

Yayıncı:

Ondokuz Mayıs University

Ana Başlıklar:

Orthopaedics

Dergi:

Deneysel ve Klinik Tıp Dergisi Vol.41 Issue 1, pp.53-59

Belge Tipi:

Makale

Yayın Tarihi:

3/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001314469

pISSN:

1309-4483

Apoptosis

Colistin

Naringin

Oxidative stress

Sciatic nerve

Sayı

Makale detayları

Naringin protects against colistin-induced sciatic nerve damage by reducing oxidative stress, apoptosis and inflammation damage

Yazarlar: Selçuk Yılmaz | Sefa Küçükler | Hasan Şimşek | Serpil Aygörmez | Fatih Mehmet Kandemir

Yayıncı: Ondokuz Mayıs University

Ana Başlıklar: Orthopaedics

Dergi: Deneysel ve Klinik Tıp Dergisi Vol.41 Issue 1, pp.53-59

Belge Tipi: Makale

Yayın Tarihi: 3/2024

Belge Dili: İngilizce

Document ID (Org No.): 2001314469

pISSN: 1309-4483

Apoptosis

Colistin

Naringin

Oxidative stress

Sciatic nerve

Sayı

Yazarlar:

Selçuk Yılmaz | Sefa Küçükler | Hasan Şimşek | Serpil Aygörmez | Fatih Mehmet Kandemir

Yayıncı:

Ondokuz Mayıs University

Ana Başlıklar:

Orthopaedics

Dergi:

Deneysel ve Klinik Tıp Dergisi Vol.41 Issue 1, pp.53-59

Belge Tipi:

Makale

Yayın Tarihi:

3/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001314469

pISSN:

1309-4483