Protective effects of camellia oils prepared with different processing conditions on NSAIDs-induced damage of gastrointestinal mucosa in vitro and in vivo
| Autor: | Ruei-Yu Wang, 王瑞宇 |
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| Rok vydání: | 2016 |
| Druh dokumentu: | 學位論文 ; thesis |
| Popis: | 104 Non-steroidal anti-inflammatory drugs (NSAIDs), including indomethacin and ketoprofen, are widely used to alleviate pain and inflammation in clinical medicine. However, these drugs may cause a damage on gastrointestinal (GI) mucosa. The previous studies indicated that digestive diseases, such as ulcers, were associated with oxidative damage in the mucosa. Phytochemicals are considered as a dietary antioxidant to possess anti-oxidantive and anti-inflammatory activities, which play an important role in GI protection. Camellia oil (Camellia oleifera Abel.) is widely used in Taiwan as cooking oil, which is rich in monounsaturated fatty acids, protein, vitamin A, vitamin E, saponin, and etc. Camellia oil has nutritional values and can be as a healthy cooking oil. The aim of this study was to evaluate the protective effects of camellia oil on NSAIDs-induced damage of gastrointestinal mucosa in an in vitro as well as in vivo, respectively. In in vitro study, our results showed that pretreatment with camellia oil or sesame oil (100 μg/mL) significantly increased the decreased cell viability by ketoprofen in gastrointestinal Int-407 cells. Moreover, camellia oil and sesame oil (75 μg/mL) also increased cell viability in indomethacin-induced Int-407 cells. Camellia oil and sesame oil (150 μg/mL) significantly decreased the generation of reactive oxygen species (ROS) in either ketoprofen or indomethacin-induced Int-407 cells. Among the tested samples, TMS camellia oil (heating treatment after pressed, 100 μg/mL) significantly inhibited the ROS production in both NSAIDs induced Int-407 cells. In ketoprofen-induced model, TML camellia oil (150 μg/mL) significantly enhanced HO-1 mRNA expression; however, in the indomethacin-induced model, the TMS and KRL (150 μg/mL) elevated the HO-1 mRNA expression but TML significantly enhanced HO-1 mRNA expression at concentration of 150 μg/mL. As mentioned above, TMS camellia oil possessed the most efficacy on gastrointestinal protection. Camellia oil increased protein expressions of antioxidant enzyme HO-1 and growth factor VEGF in Int-407 cells. In in vivo experiment, pretreatment of BALB/c mice with camellia oil (1 and 2 mL/kg) for 21 days prior to the administration of indomethacin (40 mg/kg) markedly inhibited inflammatory COX-2, IL-6 and TNF-α expression. Increasing protein expression HO-1 expression and VEGF in mice was regulated by camellia oil administration. Most importantly, pretreatment of mice with camellia oil (1 and 2 mL/kg) inhibited the induction of gastric mucosal damage caused by indomethacin, as compared to the lansoprazole group, which was demonstrated by the histopathological staining of stomach tissues. In conclusion our results support the possible use of camellia as a dietary functional oil against oxidative damage of gastric mucosa. |
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