Ibuprofen is an anti-inflammatory agent targeting COX-1 and COX-2 with IC₅₀s of 13 μM and 370 μM, respectively.

Ibuprofen inhibits the enzyme cyclooxygenase COX-1 and COX-2, which convert arachidonic acid to prostaglandin H2 (PGH2). Its action is similar to aspirin, indomethacin and all other NSAIDs in intact cells, broken cells, and purified enzyme preparations^[1]. Ibuprofen inhibits the constitutive activation of NF-κB and IKKα in the androgen-independent prostate tumor cells PC-3 and DU-145. It sensitizes prostate cells to ionizing radiation and blocks stimulated activation of NF-κB following exposure to TNFα or ionizing radiation in the androgen-sensitive prostate tumor cell line LNCaP. Both of these cannot be attributed directly to inhibition of IκB-α kinase but to inhibition of an upstream regulator of IKKα^[2]. Ibuprofen exerts an anticancer effect by reducing survival of cancer cells. Ibuprofen is more efficacious than aspirin and acetaminophen, and comparable with (R)-flurbiprofen and indomethacin in induction of p75NTR protein expression in cell lines from bladder and other organs^[3].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Ibuprofen reacts with the heme group of cyclooxygenase to prevent arachidonic acid conversion. Prior exposure to Ibuprofen in vivo protects cyclooxygenase completely from the irreversible effects of aspirin in platelets^[4]. Ibuprofen treatment is effective in attenuating joint inflammation and early articular cartilage degeneration in the adult female Sprague-Dawley rat model induced by high-repetition and high-force (HRHF) task. It dose this by blocking the increases in serum C1 and 2C (a biomarker of collagen I and II degradation) as well as the ratio of collagen degradation to synthesis (C1, 2C/CPII, the latter a biomarker of collage type II synthesis) induced by HRHF^[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

206.28

C₁₃H₁₈O₂

15687-27-1

布洛芬；异丁苯丙酸；异丁洛芬

Room temperature in continental US; may vary elsewhere.

DMSO : 100 mg/mL (484.78 mM; Need ultrasonic)

H₂O : 1 mg/mL (4.85 mM; Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.5 mg/mL (12.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (12.12 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.5 mg/mL (12.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (12.12 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (12.12 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (12.12 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Noreen Y, et al. Development of a radiochemical cyclooxygenase-1 and -2 in vitro assay for identification of natural products as inhibitors of prostaglandin biosynthesis. J Nat Prod. 1998 Jan;61(1):2-7.

  [2]. Palayoor ST, et al. Constitutive activation of IkappaB kinase alpha and NF-kappaB in prostate cancer cells is inhibited by ibuprofen. Oncogene. 1999 Dec 2;18(51):7389-94.

  [3]. Khwaja F, et al. Ibuprofen inhibits survival of bladder cancer cells by induced expression of the p75NTR tumor suppressor protein. Cancer Res. 2004 Sep 1;64(17):6207-13.

  [4]. Rao GH, et al. Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. Arteriosclerosis. 1983 Jul-Aug;3(4):383-8.

  [5]. Driban JB, et al. Joint inflammation and early degeneration induced by high-force reaching are attenuated by ibuprofen in an animal model of work-related musculoskeletal disorder. J Biomed Biotechnol. 2011;2011:691412

The number of cells in each well after treatment (48 hours) with NSAIDs is estimated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. MTT labeling reagent (final concentration, 0.5 mg/mL) is added to each of the NSAID-treated T24 cells, ponasterone A alone-treated cells, ΔDDp75NTR-transfected cells plus ponasterone A, and ΔICDp75NTR-transfected cells plus ponasterone A (2×10³ cells/well) in 96-well culture plates (final volume, 100 μL culture medium/well) and incubated for 4 hours at 37°C in a humidified atmosphere of 10% CO₂. Subsequently, cells are incubated overnight with 100 μL of solubilization solution per well, and the samples are quantified at 570 nm using a microtiter plate reader.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

At the end of the 4th week of task performance, subcohorts of the above animals are administered ibuprofen in drinking water daily (45 mg/kg body weight): NC+IBU (n=10), TR + IBU (n=11) and HRHF + IBU (n=15). HRHF+IBU animals continue to perform the HRHF task regimen with ibuprofen treatment for the remainder of the 12-week task period (i.e., an 8-week course of ibuprofen treatment). The dose used is lower than the maximum limit for gastrointestinal toxicity in rats, yet has been shown to be effective in reducing chronic inflammation. The amount of medicated water consumed/day is tracked for each animal by measuring the difference between the initial and final volume of suspended solution daily. Based on these assessments, the average weekly ibuprofen dose is similar in all groups (48.8±6.3 mg/kg body weight), with no significant differences in ibuprofen dose administered or serum levels of ibuprofen between the treated groups.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Noreen Y, et al. Development of a radiochemical cyclooxygenase-1 and -2 in vitro assay for identification of natural products as inhibitors of prostaglandin biosynthesis. J Nat Prod. 1998 Jan;61(1):2-7.

  [2]. Palayoor ST, et al. Constitutive activation of IkappaB kinase alpha and NF-kappaB in prostate cancer cells is inhibited by ibuprofen. Oncogene. 1999 Dec 2;18(51):7389-94.

  [3]. Khwaja F, et al. Ibuprofen inhibits survival of bladder cancer cells by induced expression of the p75NTR tumor suppressor protein. Cancer Res. 2004 Sep 1;64(17):6207-13.

  [4]. Rao GH, et al. Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. Arteriosclerosis. 1983 Jul-Aug;3(4):383-8.

  [5]. Driban JB, et al. Joint inflammation and early degeneration induced by high-force reaching are attenuated by ibuprofen in an animal model of work-related musculoskeletal disorder. J Biomed Biotechnol. 2011;2011:691412