thiobarbituric acid adduct formation  (Cayman Chemical)

Journal: Journal of Neuroinflammation

Article Title: Infliximab reduces Zaprinast-induced retinal degeneration in cultures of porcine retina

doi: 10.1186/s12974-014-0172-9

Figure Lengend Snippet: Infliximab partially prevents Zaprinast-induced oxidative stress in cultures of porcine retina. Retinal explants were incubated with dimethyl sulfoxide (DMSO), Zaprinast and Infliximab alone or combined with Zaprinast as described in Methods. Effect of Infliximab on the total antioxidant capacity (A) , TBARS formation (B) and intracellular NOX (C) . Each sample was measured in duplicate, and the values are the mean ±SEM of eight cultures. ANOVA Newman-Keuls post-test was used for TAC analysis. Kruskal-Wallis test and Dunn’s post-test was used for TBARS and iNOX analysis. * P <0.05, ** P <0.01. C: control; Z100: 100 μM Zaprinast; INF: 2 μg/mL Infliximab; Z100 +INF: 100 μM Zaprinast with 2 μg/mL Infliximab. iNOX, intracellular nitrites and nitrates; TAC, total antioxidant capacity; TBARS, thiobarbituric acid reactive substances.

Article Snippet: MDA levels were detected by a colorimetric method involving thiobarbituric acid (TBA) adduct formation (Cayman Chemical, Ann Arbor, MI, USA).

Techniques: Incubation, Control

Journal: Journal of Neuroinflammation

Article Title: Infliximab reduces Zaprinast-induced retinal degeneration in cultures of porcine retina

doi: 10.1186/s12974-014-0172-9

Figure Lengend Snippet: Diagram showing the possible mechanism of Infliximab in the porcine retinal degeneration model. PDE6 inhibition induces cGMP accumulation and triggers retinal degeneration. The degeneration is accompanied by upregulation of inflammatory mediators, PARP pathway, reactive gliosis and oxidative stress markers. According to the current study, TNFα may be involved in the retinal degeneration by increasing caspase-3 activation and reactive gliosis. Infliximab may prevent cell death by inhibiting caspase-dependent pathways that converge in caspase-3 activation in the INL. Infliximab also may prevent cell death by caspase-independent pathways that remain unclear in the ONL and GCL. Moreover, Infliximab may exacerbate PARP over activation probably through the caspase-3 inhibition. This over activation could contribute to the future cell death. cGMP: cyclic GMP; GCL, ganglion nuclear layer; GFAP: glial fibrillary acidic protein; INL, inner nuclear layer; NO: nitric oxide; ONL, outer nuclear layer; PAR: poly(ADP-ribose) polymers; PARG: poly(ADP-ribose) glycohydrolase; PARP: poly(ADP)ribose polymerase; PDE6: phosphodiesterase 6; TAC: total antioxidant capacity; TBARS: thiobarbituric acid reactive substances; TNFα: tumor necrosis factor alpha.

Article Snippet: MDA levels were detected by a colorimetric method involving thiobarbituric acid (TBA) adduct formation (Cayman Chemical, Ann Arbor, MI, USA).

Techniques: Inhibition, Activation Assay