Cell experiment:

Human uveal melanoma cell lines are transfected to constitutively express COX-2 and the proliferative rate of these cells using two different methods, with and without the addition of Amfenac Sodium Hydrate, is measured. Nitric oxide production by macrophages is measured after exposure to melanoma-conditioned medium from both groups of cells as well as with and without Amfenac Sodium Hydrate[1].

Amfenac Sodium Hydrate is a COX-2 inhibitor.

Cells transfected to express COX-2 have a higher proliferation rate than those do not. The addition of Amfenac Sodium Hydrate significantly decreases the proliferation rate of all cell lines. Nitric oxide production by macrophages is inhibited by the addition of melanoma conditioned medium, the addition of Amfenac Sodium Hydrate partially overcomes this inhibition[1]. Results show that Amfenac Sodium Hydrate inhibits the release of B-glucuronidase: 5×10-4 M Amfenac Sodium Hydrate inhibits the release of the enzyme 35.3 and 16.3% in the presence of 10-8, and 10-7 M FMLP, respectively. Addition of 10-4 M Amfenac Sodium Hydrate causes 28.3% inhibition of aggregation of polgmorphonuclear leukocgtes (PMNs) during incubation for 16 min with 10-8 M FMLP[2].

References:
[1]. Marshall JC, et al. The effects of a cyclooxygenase-2 (COX-2) expression and inhibition on human uveal melanoma cell proliferation and macrophage nitric oxide production. J Carcinog. 2007 Nov 27;6:17.
[2]. Matsumoto T, et al. Effect of a non-steroidal anti-inflammatory drug (amfenac sodium) on polymorphonuclear leukocytes. Pharmacol Res Commun. 1982 Jun;14(6):523-32.