RESUMO
BACKGROUND: Turmeric (Curcuma longa) L. has been recognized as a plant with high medicinal value and it has been used in the prevention and treatment of many diseases. Different studies have shown that turmeric has both therapeutic and preventive effects on peptic ulcer. However, there are controversial reports about the anti-ulcerogenic potential of turmeric. Some studies also suggested that turmeric could be ulcerogenic when consumed in large quantity with no mention of the concentration at which this could take place. AIM: This study examined the influences of different concentration of turmeric rhizome powder supplemented diet on the gene expressions of both anti-ulcer and ulcer biomarkers in indomethacin-induced ulcerated rats. METHODS: The study was conducted through prophylactic treatment of test groups with turmeric at different percentage (1%, 2%, 5%, and 10%) for 28 days. Thirty-five rats were randomly divided into seven groups namely A, B, C, D (1%, 2%, 5%, and 10% groups respectively), E (standard drug group (STD)), F (ulcerogenic group) and G (normal control group (CTL)). At the end of 28 days, rats were fasted overnight and ulcer was induced in all the groups except group G by oral administration of 60mg/kg b.w (body weight) of indomethacin. The expression of defensive (Cyclo-oxygenase-1, MUCIN, and Hyme-oxygenase-1) and destructive factors (Pepsin) were then analyzed. RESULTS: Results showed that consumption of TRPSD at 1-5% increased the gene expression of protective factors when compared with animals in group F. Furthermore, Prophylactic treatment of test groups with TRPSD at 1%-5% significantly suppressed the gene expression of pepsin in comparison with animals in group F. However, TRPSD consumption at 10% down-regulated the gene expression of those protective factors. Similarly, at 10%, pepsin gene expression was not suppressed when compared with animals in group F. Conclusively, TRPSD could be gastro protective at 1%-5%. However, these potentials were abrogated in animals in group D indicating the ulcerogenic potential of turmeric at this concentration (10%) and its capability to enhance ulcerogenic action of indomethacin. CONCLUSION: Turmeric rhizome powder (TRP) have anti-ulcerogenic potential and gastro-protective effect when consumed in appropriate concentration. Consumption of TRP at 10% concentration could enhance ulcerogenic action of indomethacin (NSAIDs) thus predisposing to ulcer. Effects of turmeric rhizome powder supplemented diet (TRPSD) on the mRNA expression of protective agents (cyclo-oxygenase-1 (COX-1), mucin, and inducible heme-oxygenase (HO-1)) and destructive factor (pepsin), in indomethacin-induced ulcerated Wistar rats were explored in this paper. These were determined by prophylactic treatment of test groups with turmeric at different levels (1%, 2%, 5%, and 10%) for 28 days. Thirty-five rats were randomly divided into seven groups namely A, B, C, D (1%, 2%, 5%, and 10% groups respectively), E (standard drug group (STD)), F (ulcerogenic group) and G (normal control group (CTL)). The rats were fasted overnight and ulcer was induced in all the groups except group G by oral administration of 60mg/kg b.w (body weight) of indomethacin. The expression of defensive (Cyclo-oxygenase-1, MUCIN, and Hyme-oxygenase-1) and destructive factors (Pepsin) were then analyzed. Results showed that consumption of TRPSD at 1%-5% increased the gene expression of protective factors when compared with animals in group F. Furthermore, Prophylactic treatment of test groups with TRPSD at 1%-5% significantly suppressed the gene expression of pepsin in comparison with animals in group F. However, TRPSD consumption at 10% down-regulated the gene expression of those protective factors. Similarly, at 10%, pepsin gene expression was not suppressed when compared with animals in group F. Conclusively, TRPSD could be gastro protective at 1%-5%. However, these potentials were abrogated in animals in group D indicating the ulcerogenic potential of turmeric at this concentration (10%) and its capability to enhance ulcerogenic action of indomethacin.