Co-administration of quercetin with pantoprazole sodium prevents NSAID-induced severe gastroenteropathic damage efficiently: Evidence from a preclinical study in rats |
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Authors: | Devendra Pratap Singh Swapnil P Borse Manish Nivsarkar |
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Institution: | 1. Department of Pharmacology and Toxicology, B.V. Patel Pharmaceutical Education and Research Development (PERD) Centre, Thaltej, Ahmedabad, Gujarat 380054, India;2. Registered Ph.D Scholar (External) at Institute of Pharmacy, NIRMA University, Sarkhej-Gandhinagar Highway, Ahmedabad, Gujarat 382481, India |
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Abstract: | Management of Nonsteroidal anti-inflammatory drug (NSAID)-induced gastroenteropathy has emerged as a major medical and socioeconomic problem mainly because the highly efficacious gastroprotective drugs i.e. proton pump inhibitors (PPIs) like pantoprazole sodium (PTZ), worsen the NSAID-induced enteropathic damage and lack of approved therapeutic strategies/interventions to prevent this damage. Hence, the primary objective of the current study was to assess whether we can protect the GI mucosa against gastroenteropathic damage caused by diclofenac sodium (DIC) in rats by co-administration of PTZ and quercetin (QCT). Rats were treated twice daily with QCT (35, 50 and 100 mg kg?1 peroral) and/or PTZ (4 mg kg?1) or vehicle for a total of 10 days. In some experiments, DIC (9 mg kg?1) was administered orally twice daily for the final 5 days of PTZ/QCT + PTZ/vehicle administration. Rats in all the groups were fasted after the last dose on 9th day, but, water was provided ad libitum. 12 h after the last dose on 10th day, rats were euthanized and their GI tracts were assessed for haemorrhagic damage, lipid peroxidation, intestinal permeability and GI luminal pH alterations along with haematological and biochemical estimations. The experimental evidences suggested that co-administration of QCT with PTZ significantly attenuated the exacerbation of NSAID-induced enteropathic damage in a dose dependent manner. The combination of PTZ 4 mg kg?1 and QCT at the doses of 50 or 100 mg kg?1 was found to effective in preventing the DIC-induced gastroenteropathy. The present report focuses on the gastroenteroprotective ability of QCT and the mechanisms may be related to its ability to prevent GI blood loss, the lipid peroxidation, intestinal permeability alteration and alteration in GI luminal pH. |
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Keywords: | DIC diclofenac sodium Hb haemoglobin HCT haematocrit H2RAs histamine H2 receptor antagonists IP intestinal permeability LPO lipid peroxidation NSAIDs nonsteroidal anti-inflammatory drugs PPIs proton pump inhibitors QCT quercetin ROS Reactive oxygen species Nonsteroidal anti-inflammatory drugs Quercetin Ulcers Enteropathy gastroenteropathy Permeability Rats |
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