Cardiovascular diseases are one of the leading causes of death worldwide. They have diverse causes such as atherosclerosis, hypertension, and unhealthy lifestyle. Atherosclerosis is also known as arteriosclerotic vascular disease (ASVD) and is commonly referred as hardening or furring of the arteries. It is characterized by thickening of artery wall due to the accumulation of fatty substances, e.g. cholesterol. This condition involves chronic inflammatory response in the walls of arteries as a result of accumulation of macrophages (white blood cells) promoted by low-density lipoproteins.
Studies carried out with Tetrahydrocurcuminoids (THCs) showed its potential as a cardiovascular protecting agent. In a study on rabbits, it was found that Tetrahydrocurcumin (THC) was able to reduce the atherosclerotic lesions area (Natio et al., 2002).
In another study, the cardioprotective effects of THC and rutin were evaluated using ischemia-reperfusion (I/R) injury model of myocardial infarction (MI) in male rats. MI-I/R injury resulted in significant cardiac necrosis, elevation of lipid peroxidation, elevation of cardiac marker enzymes e.g., aspartate aminotransferase (AST), alanine aminotransferase (ALT) as well as decreased the antioxidant status viz., catalase, reduced glutathione in the normal control MI-I/R group and vehicle control MI-I/R group. The THC and rutin showed significant reduction in MI-I/R injury caused infarct (necrosis) size compared to control group. Further, MI-I/R-induced lipid peroxidation was also significantly inhibited by THC and rutin. Thus the suppression of oxidative stress by THC and rutin was suggested as the possible mode of cardio-protection as confirmed by histopathological examination (Ali et al., 2009).
An in vitro study compared several antioxidants for their efficacy to prevent the formation of trans-isomers of arachidonic acid induced by thiyl radicals generated by ultraviolet (UV) irradiation of 2-mercaptoethanol. It was found that THC topped the list as a preventive agent like that of curcumin and resveratrol (Hung et al., 2011).
Inhibitory effects of antioxidants on thiyl radical-induced TAA (trans-arachidonic acid) formation
(Adapted from Hung et al., 2011)
| Antioxidants | all-cis | mono-trans | di-trans | tri-trans | all-trans | inhibition(%) |
|---|---|---|---|---|---|---|
| Control | 24.43 ± 0.99 | 30.49 ± 2.35 | 25.31 ± 1.17 | 14.64 ± 1.70 | 5.13 ± 0.99 | 0.00 ± 0.00 |
| Curcumin | 57.34 ± 1.42 | 24.08 ± 0.94 | 11.41 ± 0.50 | 5.46 ± 0.18 | 1.71 ± 0.14 | 45.53 ± 2.38 |
| Tetrahydrocurcumin | 56.11 ± 4.71 | 25.70 ± 5.59 | 11.51 ± 0.65 | 4.55 ± 1.73 | 2.12 ± 0.94 | 41.86 ± 6.87 |
| Resveratol | 54.88 ± 3.02 | 25.97 ± 1.86 | 12.59 ± 1.04 | 5.19 ± 0.64 | 1.37 ± 0.29 | 40.32 ± 3.20 |
| α-tocopherol | 43.25 ± 1.51 | 29.53 ± 1.53 | 16.56 ± 0.41 | 7.81 ± 0.48 | 2.85 ± 0.52 | 24.90 ± 1.36 |
| Retinol acetate | 42.78 ± 3.38 | 30.57 ± 2.67 | 16.34 ± 1.13 | 7.30 ± 0.08 | 3.01 ± 1.16 | 24.31 ± 3.50 |
| Ascorbic acid | 40.23 ± 4.13 | 30.02 ± 3.51 | 18.55 ± 1.73 | 8.21 ± 0.81 | 3.00 ± 1.15 | 20.90 ± 5.57 |
| Gallic acid | 37.56 ± 4.51 | 27.81 ± 4.47 | 21.20 ± 1.75 | 10.09 ± 1.11 | 3.34 ± 1.80 | 17.31 ± 7.00 |
| Sesamol | 37.03 ± 4.53 | 31.12 ± 1.72 | 19.56 ± 1.51 | 8.62 ± 1.91 | 3.68 ± 1.46 | 16.63 ± 6.56 |