阿斯匹靈屬於非類固醇抗發炎藥的ㄧ種,會造成胃黏膜損傷,甚至引起胃、十二指腸潰瘍與其他併發症。已有研究證實活性氧自由基產生,胃黏膜的抗氧化能力減弱是造成傷害的原因之一。在先前的研究中發現龍葵成份已有多項抗氧化之報告,因此本研究目的在於如何利用龍葵水萃取物 (Solanum nigrum water extract, SNE)回復抗氧化酵素的活性而降低aspirin誘發胃黏膜損傷的風險。動物模式為以管餵預先處理SNE (100 mg/kg ;200 mg/kg ;400 mg/kg )一小時後,再管餵食200 mg/kg的aspirin,經四小時誘導Wistar大白鼠產生胃黏膜損傷。由結果發現預先處理龍葵水萃取物能降低血液中白血球的數目,也能降低胃黏膜MDA的量,同時也發現預先餵食龍葵水萃物的老鼠能回復由aspirin所減少的total GST, GST Ai, GST Pi與GSH量,利用western blot發現處理SNE能降低由aspirin所誘導的COX-2表現,綜合以上的結果,我們認為龍葵水萃物應能透過調節胃黏膜抗氧化狀態以預防aspirin誘導的胃黏膜損傷。
A recent study demonstrated that long-term use of aspirin, a none-steroidal anti-inflammatory drug (NSAID), will cause gastric mucosal damage, gastro-duodenal ulcers and complication. The cause could be due to aspirin induced reactive oxygen species (ROS) and decreased gastric mucosal antioxidant activity. We previously showed Solanum nigrum water extract (SNE) possessed antioxidative activities. In this study, we tried to detect the protective effect of SNE in aspirin inducing gastric mucosal damage. Animals were pretreated with SNE (100 mg/kg, 200 mg/kg, 400 mg/kg) for 1 hour, and then 200 mg/kg of aspirin was oral-fed to induce gastric mucosal lesions. After 4 hours, the animals were sacrificed to perform the following detections. We observed that SNE can reduce the white blood cell and the contents of malondialdehyde (MDA) in the gastric mucosa. SNE can also recover antioxidant enzyme activities such as total GST, GST Ai, GST Pi and GSH which were decreased by aspirin. In conclusion, SNE protects aspirin-induced gastric mucosal damage could be via regulating anti-oxidative enzyme activities and reducing the damage of ROS.