Abstract
It is well known that Phellinus linteus, which produces hispidin and its derivatives, possesses antioxidant activities. In this study, we investigated whether hispidin has protective effects on palmitate-induced oxidative stress in C2C12 skeletal muscle cells. Our results showed that palmitate treatment in C2C12 myotubes increased ROS generation and cell death as compared with the control. However, pretreatment of hispidin for 8 h improved the survival of C2C12 myotubes against palmitate-induced oxidative stress via inhibition of intracellular ROS production. Hispidin also inhibited palmitate-induced apoptotic nuclear condensation in C2C12 myotubes. In addition, we found that hispidin can suppress cleavage of caspase-3, expression of Bax, and NF-κB translocation. Therefore, these results suggest that hispidin is capable of protecting C2C12 myotubes against palmitate-induced oxidative stress.
Highlights
Insulin resistance is recognized as a major risk factor for type 2 diabetes mellitus, and it is characterized by the reduced ability of insulin to regulate glucose homeostasis in target tissues, such as muscle, liver, and adipose [1,2]
It is well known that elevation in plasma free fatty acids (FFAs) levels is commonly associated with impaired insulin-mediated glucose uptake in skeletal muscles [5,6]
MTT assays showed that there was no significant change in cell viability after treatment with hispidin at concentrations from 1 to 100 μM (Figure 1A)
Summary
Insulin resistance is recognized as a major risk factor for type 2 diabetes mellitus, and it is characterized by the reduced ability of insulin to regulate glucose homeostasis in target tissues, such as muscle, liver, and adipose [1,2] Among these target tissues, skeletal muscle is responsible for more than 75% of glucose disposal in response to insulin in the post-prandial state [3,4]. Excessive generation of ROS, such as superoxide anion and hydroxyl radical, initiates the mitochondria-mediated apoptotic pathway by altering the expression of Bcl-2 family proteins, thereby increasing the mitochondrial transmembrane potential, affecting mitochondrial membrane integrity, and releasing cytochrome c [18]. In this study, we investigate whether the antioxidant activity of hispidin has a cytoprotective effect against palmitate-induced lipotoxicity
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