It has been reported that some of the food additives may cause sensitization, inflammation of tissues, and potentially risk factors in the development of several chronic diseases. Thus, we hypothesized that expressions of common inflammatory molecules -known to be involved in the development of various inflammatory conditions and cancers -are affected by these food additives. We investigated the effects of commonly used food preservatives and artificial food colorants based on the expressions of NFκB, GADD45α, and MAPK8 (JNK1) from the tissues of liver. RNA was isolated based on Trizol protocol and the activation levels were compared between the treated and the control groups. Tartrazine alone could elicit effects on the expressions of NFκB (p = 0.013) and MAPK8 (p = 0.022). Azorubine also resulted in apoptosis according to MAPK8 expression (p = 0.009). Preservatives were anti-apoptotic in high dose. Sodium benzoate (from low to high doses) dose-dependently silenced MAPK8 expression (p = 0.004 to p = 0.002). Addition of the two preservatives together elicited significantly greater expression of MAPK8 at half-fold dose (p = 0.002) and at fivefold dose (p = 0.008). This study suggests that some of the food preservatives and colorants can contribute to the activation of inflammatory pathways.

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Background Healthy functioning of the brain requires a precise autoregulation of cerebral blood flow, which in part is achieved by the pressure and flow sensitive vasomotor mechanisms. Traumatic brain injury (TBI) frequently occurs worldwide, resulting in brain diseases with high morbidity and mortality. Here, we hypothesized that TBI impairs the autoregulatory mechanisms, namely the pressure‐ and flow‐induced constrictions of isolated rat middle cerebral arteries (MCAs). Methods TBI was induced in anaesthetized rats by weight drop model, and then MCAs were isolated and transferred into a pressure‐flow chamber. Changes in internal diameter in response to hemodynamic forces and vasoactive drugs were measured by a video‐microscopy. Results In MCAs from intact rats, increases in pressure‐, flow‐ and pressure + flow elicited constrictions (max.: ‐26 ± 1.7; ‐26 ± 1.9; and ‐52 ± 2.8 µm, p < 0.05). Flow‐induced constrictions were significantly reduced by HET0016, an inhibitor of cytochrome P450 4A (CYP450 4A) or in the presence of thromboxane‐prostanoid (TP receptor) antagonist SQ 29,548. Both responses were significantly reduced after TBI. Arachidonic acid, (AA, 10−7 M), and CYP450 4A metabolite 20‐hydroxyeicosatetraenoic acid (20‐HETE) elicited constrictions of intact MCA (‐26 ± 2.3% and ‐31 ± 3.6%), which were significantly reduced after TBI (to ‐11 ± 1.3% and ‐16 ±2.5%). The TP receptor agonist U46619 (10−7 M) elicited substantial constrictions of MCA from intact rats (‐21 ± 3.3%), which were also significantly reduced, after TBI (to ‐16 ± 2.4%). Conclusions Both pressure and flow‐induced constrictions of MCA were impaired by traumatic brain injury, likely due to the reduced ability of cytochrome P450 4A to convert arachidonic acid to constrictor prostaglandins (cPGs) and the mitigated sensitivity of thromboxane‐prostanoid receptors to cPGs. We propose that the impairment of autoregulatory vasomotor mechanisms contribute to the TBI‐induced human brain diseases, such as headache, disruption of blood brain barrier, brain edema, Alzheimer‐type diseases and vascular dementia.