Analgesic Effects and the Mechanisms of Anti-inflammation of Ergostatrien-3β-ol from Antrodia camphorata Submerged Whole Broth in Mice
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- 作者：Guan-Jhong Huang ; Shyh-Shyun Huang ; Shiang-Shiou Lin ; Yi-Yuan Shao ; Chin-Chu Chen ; Wen-Chi Hou ; Yueh-Hsiung Kuo
- 刊名：Journal of Agricultural and Food Chemistry
- 出版年：2010
- 出版时间：June 23, 2010
- 年：2010
- 卷：58
- 期：12
- 页码：7445-7452
- 全文大小：937K
- 年卷期：v.58,no.12(June 23, 2010)
- ISSN：1520-5118
文摘
Ergostatrien-3β-ol (ST1), an active and major ingredient from Antrodia camphorata (AC) submerged whole broth was evaluated for the analgesic and anti-inflammatory effects. Treatment of male imprinting control region (ICR) mice with ST1 (1, 5, and 10 mg/kg) significantly inhibited the numbers of acetic-acid-induced writhing response in 10 min. Also, our result showed that ST1 (10 mg/kg) significantly inhibited the formalin-induced pain in the late phase (p < 0.001). In the anti-inflammatory test, ST1 (10 mg/kg) decreased the paw edema at 4 and 5 h after λ-carrageenin (Carr) administration and increased the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in the liver tissue. We also demonstrated that ST1 significantly attenuated the malondialdehyde (MDA) level in the edema paw at 5 h after Carr injection. ST1 (1, 5, and 10 mg/kg) decreased the nitric oxide (NO) levels on both the edema paw and serum level at 5 h after Carr injection. Also, ST1 (5 and 10 mg/kg) diminished the serum tumor necrosis factor (TNF-α) at 5 h after Carr injection. Western blotting revealed that ST1 (10 mg/kg) decreased Carr-induced inducible nitric oxide synthase (iNOS), and cycloxyclase (COX-2) expressions at 5 h in the edema paw. An intraperitoneal (ip) injection treatment with ST1 also diminished neutrophil infiltration into sites of inflammation, as did indomethacin (Indo). The anti-inflammatory mechanisms of ST1 might be related to the decrease in the level of MDA, iNOS, and COX-2 in the edema paw via increasing the activities of CAT, SOD, and GPx in the liver through the suppression of TNF-α and NO.