Protective effect of hesperidin against N,N'-dimethylhydrazine induced oxidative stress, inflammation, and apoptotic response in the colon of Wistar rats.

N,N′‐dimethylhydrazine apoptosis hesperidin inflammation oxidative stress

Journal

Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357

Informations de publication

Date de publication:
02 Dec 2020
Historique:
received: 11 04 2020
accepted: 20 11 2020
entrez: 8 12 2020
pubmed: 9 12 2020
medline: 9 12 2020
Statut: aheadofprint

Résumé

Hesperidin (HD), a citrus bioflavonoid possesses a variety of biological activities including antioxidant, anti-inflammatory, anti-apoptotic and anti-carcinogenic properties. In the present study, we investigated the effect of HD treatment on N,N'-dimethylhydrazine (DMH) induced oxidative stress, inflammation, apoptosis and goblet cell disintegration in the colon of Wistar rats. Administration of HD was done at two doses (100 and 200 mg/kg body weight) orally to rats daily for 14 days followed by a single subcutaneous injection of DMH (40 mg/kg body weight) on the 14th day and next day animals were sacrificed. The protective potential of HD against colon toxicity was measured through membrane oxidation, antioxidant status, inflammatory and apoptotic markers expression, and histological changes. Results demonstrated that HD inhibited DMH mediated oxidative damage by diminishing the level of peroxidation of lipids and increasing the activity of superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, glutathione-s-transferase, and glutathione reductase. Moreover, HD attenuated inflammatory (NF-кB, IL-6, and COX-2) and apoptotic (p38-MAPK, p53, and caspase-3) markers expression. HD also attenuated the DMH induced goblet cell disintegration and restored histoarchitecture of the colon. The results of the present study demonstrate that HD efficiently protects against DMH induced colon toxicity by modulating oxidative stress, inflammation, and apoptosis.

Identifiants

pubmed: 33289288
doi: 10.1002/tox.23068
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2020 Wiley Periodicals LLC.

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Auteurs

Shekh Mohammad Afzal (SM)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Abul Vafa (A)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Summya Rashid (S)

Department of Pharmacology and Toxicology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia.

Preeti Barnwal (P)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Ayaz Shahid (A)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Alpa Shree (A)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Johirul Islam (J)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Nemat Ali (N)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.

Sarwat Sultana (S)

Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology & Toxicology, School of Chemical and Life Sciences, New Delhi, India.

Classifications MeSH