Abstract
During disc degeneration, the increase of inflammatory cytokines and decrease of disc cell density are two prominent features. Enhanced inflammatory reaction contributes to disc annulus fibrosus (AF) cell apoptosis. In this study, we investigated whether resveratrol can suppress AF cell apoptosis in an inflammatory environment. Rat disc AF cells were cultured in medium with or without tumor necrosis factor-α (TNF-α). Resveratrol was added along with the culture medium supplemented with TNF-α. Caspase-3 activity, cell apoptosis ratio, expression of apoptosis-associated molecules (Bcl-2, Bax, caspase-3, cleaved PARP, and cleaved caspase-3), reactive oxygen species (ROS) content, and the total superoxide dismutase (SOD) activity were measured. Our results showed that TNF-α significantly increased caspase-3 activity and AF cell apoptosis ratio and upregulated gene/protein expression of Bax, caspase-3, cleaved caspase-3, and cleaved PARP, whereas it downregulated the expression of Bcl-2. Moreover, TNF-α significantly increased ROS content but decreased the total SOD activity. Further analysis demonstrated that resveratrol partly attenuated the effects of TNF-α on AF cell apoptosis-associated parameters, decreased ROS content, and increased the total SOD activity in the AF cells treated with TNF-α. In conclusion, resveratrol attenuates inflammatory cytokine TNF-α-induced AF cell apoptosis through regulating oxidative stress reaction in vitro. This study sheds a new light on the protective role of resveratrol in alleviating disc degeneration.
Highlights
IntroductionIntervertebral disc degeneration (IDD) is a main contributor to low back pain and the procession of disc herniation
Low back pain is a debilitating disorder that occurs in ~70% of the population [1]
When resveratrol was added into the medium of the tumor necrosis factor-α (TNF-α) group, annulus fibrosus (AF) cell apoptosis ratio was partly decreased (Figure 1)
Summary
Intervertebral disc degeneration (IDD) is a main contributor to low back pain and the procession of disc herniation. This kind of disease often affects life quality of adults and has a tremendous socioeconomic impact [2, 3]. Several previous studies have showed that excessive apoptosis-induced loss of disc cells plays a key role in the disc degeneration process [5, 6]. Lots of studies have reported an increase in the expression of apoptotic genes (Bax and caspase-3/9) and a decrease in the expression of antiapoptotic gene (Bcl-2) in patients with disc degeneration [10, 11]
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