TO ASSESS THE POTENTIAL OF CURCUMIN AGAINST GUT MICROBIOTA-INDUCED ALTERATION IN CHOLINE METABOLISM IN C57BL/6J MICE

摘要

Objective: The present study was focused on assessing the antimicrobial activity of curcumin against Providencia rettgeri, a gut microbe, which was further corelated to the effect of curcumin on choline metabolism and its role in preventing atherosclerosis and on the evaluation of potential of curcumin on the inhibition of conversion of choline to trimethylamine (TMA), and further its conversion to trimethylamine-N-oxide (TMAO) in liver. Methods: The minimum inhibitory concentration of curcumin was determined using Cup-plate method. The estimation of trimethylamine was performed using high performance thin layer chromatography (HP-TLC) technique. Estimation of blood serum parameters were performed using kits supplied by Span-diagnostics for estimation of triglycerides, total cholesterol and high density lipoprotein (HDL) cholesterol. All surgical procedures on animals including blood withdrawal and isolation of livers were carried out in accordance with CPCSEA guidelines. Results: The minimum inhibitory concentration of curcumin was found to be 10 μg/ml. There was a significant increase (p<0.001) in the mean triglyceride, total cholesterol, low-density and very low-density lipoprotein, along with a significant decrease (p<0.001) in high-density lipoprotein in choline-fed mice. Also, there was significant decrease (p<0.001) in the mean triglyceride, total cholesterol, low-density and very low-density lipoprotein, along with a significant increase (p<0.001) in high-density lipoprotein cholesterol in choline-fed mice treated with curcumin. Further, there was a decrease in the Flavin mono-oxygenase (FMO 3 ) activity in the mice livers treated with curcumin by 21.57%. Conclusion: It was concluded that curcumin has the potential to inhibit gut microbiota thus prevention the conversion of choline to trimethylamine, has serum lipid lowering effect in female C57BL/6J mice and has an inhibitory effect on hepatic FMO 3 thus preventing the conversion of trimethylamine to trimethylamine-N-oxide.