包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
10mg | 电议 |
50mg | 电议 |
100mg | 电议 |
Animal experiment: | Mice[2]Briefly, male ddy mice weighing about 30 g are used. The writhing syndrome is induced by injecting 0.75% of acetic acid, intraperitoneally. Ten minutes later, the number of writhings are counted for the next 10 min. NS-398 is administered orally 30 min prior to the injection. The analgesic effect is expressed as % of inhibition, compared with the vehicle-treated control[2].Rats[2]Briefly, male Lewis rats weighing about 160 g are used. Arthritis is induced by injecting 0.1 mL of 0.7% Mycobacterium tubercu-losis-liquid paraffin into the left hind paw. On day 15, the rats are grouped according to the degree of secondary lesions in the right hind paw. NS-398 is administered orally once daily from days 15 to 18. Foot volume is measured on day 19. Relative edema volume (REV) is calculated for each animal[2]. |
产品描述 | NS 398 is a selective inhibitor of cyclooxygenase-2 with IC50 value of 3.8 μM [1]. Cyclooxygenase (COX) is an enzyme that is responsible for the formation of prostaglandins, prostacyclin and thromboxane. COX-2 converts arachidonic acid (AA) to prostaglandin endoperoxide H2. NS 398 is a selective COX-2 inhibitor and a novel anti-inflammatory agent. NS 398 inhibited COX-2 with IC50 value of 3.8 μM in a concentration-dependent way [1]. In RG/C2, AA/C1 and RR/C1 pre-malignant human colorectal adenoma cell lines, NS-398 (20 ~ 100 μM) inhibited cell proliferation and induced apoptosis. In HT29 colorectal carcinoma cell lines, NS-398 induced apoptosis. Also, NS-398 increased COX-2 protein expression. In HT29 cultures, NS-398 inhibited prostaglandin E2 secretion and COX-2 activity [2]. In rats with trauma, NS-398 (0.3-5 mg/kg) exhibited anti-inflammatory and analgesic effects [1]. In Balb/C mice, NS-398 (10 mg/kg) reduced prostaglandin E2 (PGE2) production and also significantly decreased the production of NO, IL-6 and TNF-α. Also, NS-398 decreased the mRNA levels of COX-2 and inhibited NF-κB activation. These results suggested that NS-398 regulated the inflammatory response after trauma and improved survival [3]. References: |