Abstract

Andrographis paniculata (Burm.f.) has long been used in ayurvedic medicine through its anti-inflammatory properties. However, its protective effect of skin aging has not been studied in vitro. This study aimed to investigate the anti-aging effects of methanolic extract (ME), andrographolide (ANDRO), neoandrographolide (NEO), 14-deoxyandrographolide (14DAP) and 14-deoxy-11,12-didehydroandrographolide (14DAP11-12) on human dermal fibroblasts (HDFa) under pro-oxidant or pro-inflammatory condition. The in vitro anti-aging capacity of ME, ANDRO, NEO, 14DAP, and 14DAP11-12 (1, 2.5 and 5 µg/mL) was performed in HDFa. Oxidative stress and inflammation were induced by hydrogen peroxide and lipopolysaccharide/TNF-α, respectively. Reactive oxygen species (ROS) production was measured by the fluorescence of DCF-DA probe and cytokines were quantified by ELISA (IL6 and IL8) or RTqPCR (TNF-α). Procollagen type I production was determined by an ELISA. Our results showed a decrease in ROS production with ME and 14DAP at 5 µg/mL and 1 µg/mL, respectively. Furthermore, IL-6 production and TNF-α expression decreased under ANDRO and ME at 5 µg/mL. Our data indicated that ME and 14DAP protect from oxidative stress. Additionally, ME and ANDRO decreased an inflammation marker, IL-6. This suggests their potential natural treatment against skin damage. Hence, their applications could be of interest in cosmetics for preventing skin ageing.

Highlights

  • Skin aging is a complex and unavoidable process

  • We focused on Andrographis paniculata (Burm.f.), which is part of the Acanthaceae family

  • ANDRO was identified in our extract of Andrographis paniculata

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Summary

Introduction

Skin aging is a complex and unavoidable process. It is divided into two categories: intrinsic aging and extrinsic aging. Antioxidants 2020, 9, 432 associated with reactive oxygen species (ROS) production that exceeds the antioxidant defenses [3,4] This imbalance causes oxidative stress in cells. An excess of ROS induced by UV radiation can activate the IkB kinase, which leads to the phosphorylation IkB and to the activation of NF-κB [8,9]. This activation induces pro-inflammatory cytokine secretion, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) [10,11]

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