Ixora parviflora Protects against UVB-Induced Photoaging by Inhibiting the Expression of MMPs, MAP Kinases, and COX-2 and by Promoting Type I Procollagen Synthesis.

Ixora parviflora with high polyphenol content exhibited antioxidant activity and reducing UVB-induced intracellular reactive oxygen species production. In this study, results of the photoaging screening experiments revealed that IPE at 1000 µg/mL reduced the activity of bacterial collagenase by 92.7 ± 4.2% and reduced the activity of elastase by 32.6 ± 1.4%. Therefore, we investigated the mechanisms by which IPE exerts its anti-photoaging activity. IPE at 1 µg/mL led to an increase in type I procollagen expression and increased total collagen synthesis in fibroblasts at 5 µg/mL. We found that IPE inhibited MMP-1, MMP-3, and MMP-9 expression at doses of 1, 5, and 10 µg/mL, respectively, in fibroblasts exposed to UV irradiation (40 mJ/cm(2)). Gelatin zymography assay showed that IPE at 50 µg/mL inhibited MMP-9 secretion/activity in cultured fibroblasts after UVB exposure. In addition, IPE inhibited the phosphorylation of p38, ERK, and JNK induced by UVB. Furthermore, IPE inhibited the UVB-induced expression of Smad7. In addition, IPE at 1 µg/mL inhibited NO production and COX-2 expression in UV-exposed fibroblasts. These findings show that IPE exhibits anti-inflammatory and anti-photoaging activities, indicating that IPE could be a potential anti-aging agent.

Antioxidant activity of Ixora parviflora in a cell/cell-free system and in UV-exposed human fibroblasts.

Polyphenols and flavonoids possess a variety of biological activities including antioxidant and anti-tumor activities. Ixora parviflora is a member of the flavonoid-rich Rubiaceae family of flowering plants and used as folk medicine in India. The aim of this study was to investigate the antioxidant activity of Ixora parviflora extract (IPE) in a cell-free system and erythrocytes, and the ability of IPE to inhibit reactive oxygen species (ROS) generation in human fibroblasts (Hs68) after ultraviolet (UV) exposure. Various in vitro antioxidant assays were employed in this study. The extraction yield of IPE was 17.4 ± 3.9%, the total phenolic content of IPE was 26.2 µg gallic acid equivalent (GAE)/mg leaves dry weight and the total flavonoids content was 54.2 ± 4.4 µg quercetin equvalent (QE)/mg extract. The content of chlorogenic acid was 9.7 ± 1.2 mg/g extract. IPE at 1000 µg/mL exhibited a reducing capacity of 90.5 ± 0.6%, a 1,1-diphenyl-2-picrylhydrazy (DPPH) radical scavenging activity of 96.0 ± 0.4%, a ferrous chelating activity of 72.2 ± 3.5%, a hydroxyl radical scavenging activity of 96.8 ± 1.4%, and a hydrogen peroxide scavenging activity of 99.5 ± 3.3%. IPE at 500 µg/mL also possessed inhibitory activity against 2,2'-azobis (2-methylpropionamidine) dihydrochloride (AAPH)-induced hemolysis of erythrocytes (89.4 ± 1.8%) and resulted in a 52.9% reduction in ROS generation in UV-exposed fibroblasts. According to our findings, IPE is a potent antioxidant and a potential anti-photoaging agent.

Coffea arabica extract and its constituents prevent photoaging by suppressing MMPs expression and MAP kinase pathway.

UV is a potent factor in skin photoaging and photocarcinogenesis. Therefore, investigating the inhibiting mechanisms of photoaging would be useful to enable development of agents to slow down the aging process. UV-irradiation increased metalloproteinase (MMP)-1, -3, and -9 and then causes collagen and elastin degradation, leading to the formation of coarse wrinkles and sagging skin. Polyphenols, a group of compounds, possessing a variety of biological activities including inhibition of MMP-1 and elastase, are widely distributed in plants including Coffea arabica. In this study, Coffea arabica leaves extract (CAE), its hydrolysates (CAH), chlororgenic acid and caffeic acid, are studied for their anti-photoaging effect. Coffea arabica leaves were extracted with methanol, and the extract was hydrolyzed with different concentrations of hydrochloric acid. The various concentrations of CAE, CAH, chlororgenic acid and caffeic acid were subject to MMPs and elastase inhibition tests. The fibroblast was used for collagen synthesis and MMP-1, -3, -9 inhibition tests on herbal extracts. The results showed that CAE stimulated type I procollagen expression, inhibited MMP-1, -3, -9 expression and inhibited the phosphorylation of JNK, ERK and p38. The results suggest that CAE can prevent photo-damage in skin through inhibiting MMP expression and MAP kinase pathway.