Background:
Hepatotoxicity remains an important clinical challenge. Hepatotoxicity observed in response to
toxins and hazardous chemicals may be alleviated by delivery of the curcumin in silver nanoparticles (AgNPs-curcumin). In
this study, we examined the impact of AgNPs-curcumin in a mouse model of carbon tetrachloride (CCl4)-induced hepatic
injury.
Methods:
Male C57BL/6 mice were divided into three groups (n=8 per group). Mice in group 1 were treated with vehicle
control alone, while mice in Group 2 received a single intraperitoneal injection of 1 ml/kg CCl4 in liquid paraffin (1:1 v/v).
Mice in group 3 were treated with 2.5 mg/kg AgNPs-curcumin twice per week for three weeks after the CCl4 challenge.
Results:
Administration of CCL4 resulted in oxidative dysregulation, including significant reductions in reduced glutathione
and concomitant elevations in the level of malondialdehyde (MDA). CCL4 challenge also resulted in elevated levels of
serum aspartate transaminase (AST) and alanine transaminase (ALT); these findings were associated with the destruction of
hepatic tissues. Treatment with AgNPs-curcumin prevented oxidative imbalance, hepatic dysfunction, and tissue
destruction. A comet assay revealed that CCl4 challenge resulted in significant DNA damage as documented by a 70%
increase in nuclear DNA tail-length; treatment with AgNPs-curcumin inhibited the CCL4-mediated increase in nuclear DNA
tail-length by 34%.
Conclusion:
Administration of AgNPs-curcumin resulted in significant antioxidant activity in vivo. This agent has the
potential to prevent the hepatic tissue destruction and DNA damage that results from direct exposure to CCL4.
Bilayer Edge and Curvature Effects on Partitioning of Lipids by Tail Length: Atomistic Simulations
