Abstract

Striae distensae (SD) or stretch marks are common linear scars of atrophic skin with disintegrating extracellular matrix (ECM) structures. Although fibroblasts contribute to the construction of ECM structure in SD, some studies have reported that mast cell degranulation causes the disruption of ECM in early SD lesions. Lagerstroemia indica flower (LIF) has traditionally been used in India as a diuretic. However, little is known about the effect and molecular action of Lagerstroemia indica flower extract (LIFE) on alleviating SD. This study evaluated the effects of LIFE on mast cell degranulation and the synthesis of ECM components in fibroblasts. LIFE inhibits the adhesion of rat basophilic leukemia (RBL) cells, RBL-2H3 on fibronectin (FN) and the expression of integrin, a receptor for FN, thereby reducing focal adhesion kinase (FAK) phosphorylation. In addition, LIFE attenuated the allergen-induced granules and cytokine interleukin 3 (IL-3) through the adhesion with FN. Moreover, the conditioned medium (CM) of activated mast cells decreases the synthesis of ECM components, and LIFE restores the abnormal expressions induced by activated mast cells. These results demonstrate that LIFE suppresses FN-induced mast cell activation and promotes the synthesis of ECM components in fibroblast, which indicates that LIFE may be a useful cosmetic agent for SD treatment.

Highlights

  • Striae distensae (SD) or stretch marks are common linear scars of skin

  • rat basophilic leukemia (RBL)-2H3 cells are of mucosal mast cell origin, and they are a prime model for investigating immediate hypersensitivity reactions [33,34]

  • Cytotoxicity of Lagerstroemia indica flower extract (LIFE) on a rat mucosal mast cell line, RBL-2H3, was measured by a MTT assay that measures cell metabolic activity in the cell culture

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Summary

Introduction

Striae distensae (SD) or stretch marks are common linear scars of skin. The risk factors of SD are genetic factors, hormonal excess, and mechanical stress, but the hypotheses often conflict [3,4]. SD develops pigmentation over time: the initial red linear lesions are striae rubrae (SR), while the chronic pale lesions are striae albae (SA). Histological alteration of SR shows prominent features: increase of dermal oedema between melanocytes and keratinocytes and melanogenesis in epidermis, the cleavage of collagen and the reduction or fragmentation of FN, elastin (ELN), and fibrillin (FBN), which is cross-linking, in the reticular dermis. The reorganization of collagen, FN, ELN, and FBN are thought to be a key cause in SD pathogenesis, and these genes are used as genetic markers for SD [7,8]

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