Protective effect of hesperidin against N , N ′‐dimethylhydrazine induced oxidative stress, inflammation, and apoptotic response in the colon of Wistar rats
| Autor: | Sarwat Sultana, Nemat Ali, Johirul Islam, Abul Vafa, Summya Rashid, Ayaz Shahid, Preeti Barnwal, Shekh Mohammad Afzal, Alpa Shree |
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| Rok vydání: | 2020 |
| Předmět: |
Antioxidant
Health Toxicology and Mutagenesis medicine.medical_treatment Glutathione reductase 010501 environmental sciences Management Monitoring Policy and Law Pharmacology Toxicology medicine.disease_cause 01 natural sciences Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Hesperidin 0302 clinical medicine medicine Dimethylhydrazine 0105 earth and related environmental sciences chemistry.chemical_classification biology Glutathione peroxidase General Medicine Glutathione chemistry 030220 oncology & carcinogenesis biology.protein Oxidative stress |
| Zdroj: | Environmental Toxicology. 36:642-653 |
| ISSN: | 1522-7278 1520-4081 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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