Curcumin, a component of turmeric, efficiently prevents diclofenac sodium-induced gastroenteropathic damage in rats: A step towards translational medicine

- NSAID administration resulted in significant gastroenteropathic toxicity in rats.
- Antisecretory drugs exacerbate NSAID-induced enteropathic damage.
- Curcumin prevented the NSAID-induced gastroenteropathic toxicity.
- Curcumin ensured complete GI safety against toxicity of NSAIDs.

There is a need to find/discover novel leads to treat complex and/or multi-factorial disease(s). Curcumin (CUR) is one of the promising lead molecules which need its further evaluation against NSAID-induced gastroenteropathy. Hence, the aim of the present study was to explore the pharmaco-mechanistic efficacy of CUR against NSAID-induced gastroenteropathy. Rats were treated twice daily with CUR (25, 50 and 100 mg kg−1 peroral) or vehicle for 10 days. In some experiments, diclofenac sodium (DIC; 9 mg kg−1) was administered orally twice daily for the final 5 days of CUR/vehicle administration. After the last dose on 9th day, rats were fasted. 12 h after the last dose on 10th day, rats were euthanized and their GI tracts were assessed for haemorrhagic lesions, lipid peroxidation, intestinal permeability and GI luminal pH alterations along with haemato-biochemical estimations. The macroscopic, biochemical, haematological and histological evidences suggested that co-administration of CUR resulted in dose dependent attenuation of the NSAID-induced gastroenteropathic damage and the mechanisms may be related to its ability to prevent the NSAID-induced alterations in the GI luminal pH, lipid peroxidation/oxidative stress, GI blood loss and intestinal permeability alteration. Based on these pharmaco-mechanistic results we propose it as a promising lead to treat NSAID-gastroenteropahty.