Rosmarinic acid alleviates ultraviolet‐mediated skin aging via attenuation of mitochondrial and <scp>ER</scp> stress responses

Gupta, Dhiraj; Sharma, Raghu Rai; Rashid, Haroon; Bhat, Aalim Maqsood; Tanveer, Malik A.; Abdullah, Sheikh Tasduq

doi:10.1111/exd.14773

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…Sanchez-Campillo et al suggested that rosmarinic acid may be beneficial as functional, nutraceutical and pharmaceutical product for oral administration and dermatologic photo-protective formulations. It has been reported that rosmarinic acid exhibits the effect of anti-photodamage from UVB exposure in chronic animal model (Balb/C mice) by prevention endoplasmic reticulum stress and impairment of mitochondrial dynamics via alleviation of the oxidative stress ( Gupta et al, 2023 ). Therefore, we expected that ST ethanolic extract containing rosmarinic acid would have potential effect on UVB-induced skin photodamage.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Schizonepeta tenuifolia Briq. ethanolic extract against UVB-induced skin aging and photodamage in hairless mice

Gu¹,

Lee²,

Yoo³

et al. 2023

Front. Pharmacol.

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The purpose of this study was to illuminate the mechanism by which Schizonepeta tenuifolia Briq. (ST) ethanolic extract prevents skin photoaging in HR-1 hairless mice (HR-1). The ST ethanolic extract alleviated wrinkle formation, epidermal skin thickness, and collagen degradation in skin tissues of ultraviolet B (UVB)-irradiated HR-1 mice. Expression of matrix metalloproteinases (a wrinkle-related marker) was reduced, and tissue inhibitor of metalloproteinase 1 expression was upregulated following application of ST ethanolic extract. Furthermore, skin dehydration and levels of hyaluronidase-1 and -2 (enzymes that break hyaluronic acid) were decreased. Moreover, protein expression of hyaluronan synthases (markers of skin hydration) and hyaluronic acid levels increased following ST ethanolic extract treatment in UVB-induced photoaging HR-1 mice. In addition, the phosphorylation of mitogen-activated protein kinases (MAPKs), including p38, extracellular signal-regulated kinase, and Jun N-terminal kinase was suppressed, and expression of nuclear factor-kappa was reduced. Treatment with ST ethanolic extract also reduced advanced glycation end product (AGE) accumulation and expression of the receptor for AGE (RAGE) in skin tissue. These results suggest that ST ethanolic extract moderates skin damage caused by UVB irradiation via regulating the expression of wrinkle- and hydration-related proteins, MAPKs, and RAGE.

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Section: Discussionmentioning

confidence: 99%

Protective effect of Schizonepeta tenuifolia Briq. ethanolic extract against UVB-induced skin aging and photodamage in hairless mice

Gu¹,

Lee²,

Yoo³

et al. 2023

Front. Pharmacol.

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“…Gapdh was utilized as the loading control. All the data (analyzed by the ΔΔCt method) were normalized to the control gene as described previously 26 2.10. Immunocytochemistry of MITF.…”

Section: Gene Expression Analysis (Qpcr)mentioning

confidence: 99%

(2-Methylbutyryl)shikonin Naturally Occurring Shikonin Derivative Ameliorates the α-MSH-Induced Melanogenesis via ERK1/2 and p38 MAP Kinase-Mediated Down-Regulation of the MITF Transcription Factor

Bhat,

Haroon,

Naikoo

et al. 2024

Chem. Res. Toxicol.

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Cutaneous pigmentation is an important phenotypic trait whose regulation, despite recent advances, has yet to be completely elucidated. Melanogenesis, a physiological process of melanin production, is imperative for organism survival as it provides protection against the environmental insults that majorly involve sunlight-induced skin photodamage. However, immoderate melanin synthesis can cause pigmentation disorders associated with a psychosocial impact. In this study, the hypopigmentation effect of (2-methylbutyryl)shikonin, a natural product present in the root extract of Lithospermum erythrorhizon, and the underlying mechanisms responsible for the inhibition of melanin synthesis in α-MSH-stimulated B16F10 cells and C57BL/6J mice was studied. Non-cytotoxic concentrations of (2methylbutyryl)shikonin significantly repressed cellular tyrosinase activity and melanin synthesis in both in vitro and in vivo models (C57BL/6J mice). (2-Methylbutyryl)shikonin remarkably abolished the protein expression of MITF, tyrosinase, tyrosinase-related protein 1, and tyrosinase-related protein 2, thereby blocking the production of pigment melanin via modulating the phosphorylation status of MAPK proteins, viz., ERK1/2 and p38. In addition, specific inhibition of ERK1/2 attenuated the inhibitory effects of (2methylbutyryl)shikonin on melanin synthesis, whereas selective inhibition of p38 augmented the inhibitory effect of BSHK on melanin synthesis. Moreover, topical application of (2-methylbutyryl)shikonin on C57BL/6J mouse tails remarkably induced tail depigmentation. In conclusion, with these findings, we, for the first time, report the hypopigmentation effect of (2methylbutyryl)shikonin via inhibition of cellular tyrosinase enzyme activity, subsequently ameliorating the melanin production, thereby indicating that (2-methylbutyryl)shikonin is a potential natural therapy for hyperpigmentation disorders.

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Annexin A1 protects epidermal stem cells against ultraviolet-B irradiation-induced mitochondrial dysfunction

Ge,

Chen,

Wei

2024

Arch Dermatol Res

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Rosmarinic acid alleviates ultraviolet‐mediated skin aging via attenuation of mitochondrial and ER stress responses

Cited by 4 publications

References 27 publications

Protective effect of Schizonepeta tenuifolia Briq. ethanolic extract against UVB-induced skin aging and photodamage in hairless mice

Protective effect of Schizonepeta tenuifolia Briq. ethanolic extract against UVB-induced skin aging and photodamage in hairless mice

(2-Methylbutyryl)shikonin Naturally Occurring Shikonin Derivative Ameliorates the α-MSH-Induced Melanogenesis via ERK1/2 and p38 MAP Kinase-Mediated Down-Regulation of the MITF Transcription Factor

Annexin A1 protects epidermal stem cells against ultraviolet-B irradiation-induced mitochondrial dysfunction

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