Introduction: Cadmium (Cd) is one of the major occupational and environmental toxicants, that poses serious risks to metabolic health and liver functions. This study was designed to evaluate the protective effects of aqueous extract of Curcuma longa against cadmium-induced liver damage, blood glucose imbalance and lipid profile disruptions in male Wistar albino rats.
Method: Fresh rhizomes of Curcuma longa were bought in the market and identified by a Botanist with voucher number (UNH/05/0223). They were washed, peeled and crushed and soaked with water. This was allowed to stand for a while and the sieved out to obtain the aqueous extract. A total of 42 rats were divided into 6 groups comprising of 7 each, which are: normal control, untreated cadmium group (4 mg/kg), treatment control (400 mg/kg turmeric), and three treatment groups given: low (100 mg/kg), mid (200mg/kg) and high (400 mg/kg) doses of turmeric extract. After 21 days of simultaneous cadmium induction and treatment, the rats were fasted overnight before blood was collected through the retro-orbital sinus for biochemical analyses.
Results: Phytochemical results showed the presence of these compounds in mg/100 g- alkaloids: 97.23 ± 0.68, flavonoids: 34.00 ± 2.00, terpenoids: 37.00 ± 3.60, steroids: 3.38 ± 0.18, reducing sugar: 26.66 ± 1.45, phenolics: 870.00 ± 25.19. Treatment with Curcuma longa extract showed a significant (p < 0.05) improvement in the Cd-induced disruptions in biochemical parameters most especially at mid and high doses by lowering liver enzyme markers; aspartate aminotransferase (AST), lactate dehydrogenase (LDH) as well as direct bilirubin. There was also a marked decrease in blood glucose and TAG levels with slight improvement in total cholesterol (TC), low density lipoprotein (LDL) and high density lipoprotein (HDL) when compared with the untreated group.
Conclusion: Therefore, it is concluded that aqueous extract of Curcuma longa possesses strong hepatoprotective and metabolic benefit, offering potential as a natural therapeutic agent against Cd-induced toxicity.
