Abstract
Silymarin (SMN) has been shown to possess a wide range of biological and pharmacological effects. Besides, SMN has antioxidant and free radical scavenging activities. Thioacetamide (TAA) is a well-documented liver toxin that requires oxidative bioactivation to elicit its hepatotoxic effect which ultimately modifies amine-lipids and proteins. Our study has been designed in a TAA exposed mouse model to investigate whether SMN could protect TAA-induced oxidative stress mediated hepatic and renal damage. Results suggest that TAA generated reactive oxygen species (ROS), caused oxidative stress and induced apoptosis in the liver and kidney cells via JNK as well as PKC and MAPKs signaling. All these detrimental effects of TAA could, however, be suppressed by SMN which not only scavenged ROS but also induced PI3K-Akt cell survival pathway in the liver and prevented apoptotic pathways in both the organs. Histological studies, collagen staining and DNA fragmentation analysis also supported our results. Combining, we say that SMN possess beneficial role against TAA mediated hepatic and renal pathophysiology.
Highlights
Silymarin (SMN), an extract of Silybum marianum, has well-known hepatoprotective properties (Letteron et al, 1990; Muriel and Mourelle, 1990a)
Determination of Dose and Time-Dependent Activity of SMN by alkaline phosphatase (ALP) Assay For this study, mice were randomly distributed into seven groups each consisting of six animals
The remaining five groups of animals were treated with five different doses of SMN (50, 100, 150, 200, and 250 mg/kg body weight) for 56 days after 3 weeks followed by TAA administration (Figure 1A)
Summary
Silymarin (SMN), an extract of Silybum marianum, has well-known hepatoprotective properties (Letteron et al, 1990; Muriel and Mourelle, 1990a). The vivid molecular pathways through which SMN exerts its effects are still not clear. TAA is used as a fungicide and serves as a source of sulfur in industries and pharmaceuticals (Kadir et al, 2011). Most importantly, it Abbreviations: ALP, alkaline phosphatase; ALT, alanine transaminase; AST, aspartate transaminase; CAT, catalase; GPx, glutathione peroxidase; GR, glutathione reductase; GST, glutathione S-transferase; LDH, lactate dehydrogenase; PARP, poly (ADP-ribose) polymerase 1; ROS, reactive oxygen species; SOD, superoxide dismutase
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