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. 2016 May;11(5):1987-1992.
doi: 10.3892/etm.2016.3140. Epub 2016 Mar 10.

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

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Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Ying Chen et al. Exp Ther Med. 2016 May.

Abstract

Carvedilol is a novel third generation β-blocker that acts as an antagonist of β and α adrenergic receptors, and is able to regulate various cell factors. In addition, it possesses antioxidant activity, is capable of reversing cardiac remodeling effects and has anti-arrhythmic effects. The present study aimed to investigate whether the effects of carvedilol were able to reduce conjunctivitis clinical scores. Initially, 24 Sprague Dawley (SD) rats were randomly divided into three equal groups as follows: Control group, model group and carvedilol group. The model and carvedilol group adult SD rats were injected with lipopolysaccharide (LPS) to induce conjunctivitis. In the carvedilol group, the eight SD rats with LPS-induced conjunctivitis also received 50 mg/kg/day of carvedilol for 4 weeks. Next, the effects carvedilol were assessed utilizing a system of clinical sign scores, and an enzyme-linked immunosorbent assay was used to determine the expression levels of interleukin-1β (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). Finally, nuclear factor-κB (NF-κB), nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) were analyzed by western blotting. Carvedilol was observed to significantly reduce clinical sign scores in a dose-dependent manner (P<0.01), and reduce IL-1β, IL-6, IL-8 and TNF-α expression levels (P<0.01) in the LPS-induced rat model of conjunctivitis. Carvedilol was also able to significantly reduce the protein expression levels of NF-κB, and induce the protein expression levels of NGF and VEGF in the LPS-induced rat model of conjunctivitis (P<0.01). In conclusion, the effects of carvedilol may reduce conjunctivitis clinical scores through inflammation, NGF and VEGF in LPS-induced rat models.

Keywords: carvedilol; conjunctivitis; inflammation; nerve growth factor; vascular endothelial growth factor.

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Figures

Figure 1.
Figure 1.
Chemical structure of carvedilol.
Figure 2.
Figure 2.
Effects of carvedilol on clinical sign scores in rat models of conjunctivitis. ##P<0.01 vs. control group; **P<0.01 vs. model group. Data are presented as mean ± standard deviation.
Figure 3.
Figure 3.
Effects of carvedilol on (A) IL-1β (B) IL-6 (C) IL-8 and (D) TNF-α in a rat model of conjunctivitis. ##P<0.01 vs. control group; **P<0.01 vs. model group. Data are presented as mean ± standard deviation. IL, interleukin; TNF-α, tumor necrosis factor-α.
Figure 4.
Figure 4.
Effects of carvedilol on NF-κB protein expression levels in a rat model of conjunctivitis using (A) western blot analysis and (B) statistical analysis. ##P<0.01 vs. control group; **P<0.01 vs. model group. Data are presented as mean ± standard deviation. NF-κB, nuclear factor-κB.
Figure 5.
Figure 5.
Effects of carvedilol on NGF protein expression levels in a rat model of conjunctivitis using (A) western blotting assays and (B) statistical analysis. ##P<0.01 vs. control group; **P<0.01 vs. model group. Data are presented as mean ± standard deviation. NGF, nerve growth factor.
Figure 6.
Figure 6.
Effects of carvedilol on VEGF protein expression levels in a rat model of conjunctivitis using (A) western blotting assays and (B) statistical analysis. ##P<0.01 vs. control group; **P<0.01 vs. model group. Data are presented as mean ± standard deviation. VEGF, vascular endothelial growth factor.

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