We are analyzing https://link.springer.com/article/10.1007/s10787-022-01041-8.

Title:
Modulation of autophagy, apoptosis and oxidative stress: a clue for repurposing metformin in photoaging | Inflammopharmacology
Description:
Long-term sun exposure is the commonest cause of photoaging, where mutual interplay between autophagy, oxidative stress, and apoptosis is incriminated. In combating photoaging, pharmacological approaches targeted to modulate autophagy are currently gaining more ground. This study aimed to examine repurposing metformin use in such context with or without the antioxidant coenzyme Q10 (coQ10) in ultraviolet A (UVA) irradiation-induced skin damage. The study was conducted on 70 female CD1 mice that were randomly assigned into seven groups (10/group): normal control, vehicle-treated-UVA-exposed mice, three metformin UVA-exposed groups (Topical 1 and 10%, and oral 300 mg/kg), topical coQ10 (1%)-treated mice, and combined oral metformin with topical coQ10-treated UVA-exposed mice. After UVA-exposure for 10 weeks (3 times/week), macroscopic signs of photoaging were evaluated. Mice were then euthanized, and the skin was harvested for biochemical estimation of markers for oxidative stress, inflammation, matrix breakdown, and lysosomal function. Histopathological signs of photoaging were also evaluated with immunohistochemical detection of associated changes in autophagic and apoptotic markers. Metformin, mainly by topical application, improved clinical and histologic signs of photoaging. This was associated with suppression of the elevated oxidative stress, IL-6, matrix metalloproteinase 1, and caspase, with induction of cathepsin D and subsequent change in anti-LC3 and P62 staining in skin tissue. In addition to metformin antioxidant, anti-inflammatory, and antiapoptotic activities, its anti-photoaging effect is mainly attributed to enhancing autophagic flux by inducing cathepsin D. Its protective effect is boosted by coQ10, which supports their potential use in photoaging.
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Keywords {🔍}

metformin, skin, autophagy, pubmed, uva, article, mice, google, scholar, dermal, versus, photoaging, met, coq, cas, group, effect, cells, normal, oral, control, topical, staining, treatment, observed, central, cathepsin, oxidative, significant, coenzyme, autophagic, cell, keratinocytes, positive, exposure, uvaexposed, fig, increase, analysis, data, treated, fibroblasts, drug, mmp, signs, expression, epidermal, antibody, combined, reduced,

Topics {✒️}

vehicle-treated-uva-exposed mice vehicle-treated uva-exposed mice targeting nuclear factor-κb vehicle-uva-exposed mice revealed article download pdf metformin-treated uva-exposed groups stress-induced cell death uva-exposed mice versus treated uva-exposed mice lead acetate-induced neurotoxicity analytical-grade commercial products vehicle-uva-exposed group uva-exposed mice supporting veh-treated uva group vehicle-uva-exposed mice uva-exposed mice showed uv radiation-induced damage uva-induced photoaged mice photoaging-induced cutaneous elastin coq10-treated groups versus uv-induced skin damage drug-treated groups approaching combined-treatment group versus probable dose-dependent effect 12% sds-page mini-gel aging-related signaling pathways mitogen-activated protein kinases metformin uva-exposed groups inhibits il-1α production long-lived differentiated cells autophagic-lysosomal dysregulation downstream mediates auto-lysosomal degradation mitochondrial respiratory chain short-lived differentiated keratinocytes autophagy-activating skincare regimen death factor bax al-mouassat medical campus anti-caspase-stained cells micro/macro-scopic signs uvb-irradiated hacat cells lc3-ii positive cells uv-stimulated human keratinocytes major counter-regulatory process significantly increased lc3-ii irradiation-induced skin damage coenzyme q10 protects combined met oral + coq10 full access dalia kamal mostafa immuno-stained sections

Questions {❓}

Klimova B, Novotny M, Kuca K (2018) Anti-aging drugs—prospect of longer life?

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WebPage:
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         description:Long-term sun exposure is the commonest cause of photoaging, where mutual interplay between autophagy, oxidative stress, and apoptosis is incriminated. In combating photoaging, pharmacological approaches targeted to modulate autophagy are currently gaining more ground. This study aimed to examine repurposing metformin use in such context with or without the antioxidant coenzyme Q10 (coQ10) in ultraviolet A (UVA) irradiation-induced skin damage. The study was conducted on 70 female CD1 mice that were randomly assigned into seven groups (10/group): normal control, vehicle-treated-UVA-exposed mice, three metformin UVA-exposed groups (Topical 1 and 10%, and oral 300 mg/kg), topical coQ10 (1%)-treated mice, and combined oral metformin with topical coQ10-treated UVA-exposed mice. After UVA-exposure for 10 weeks (3 times/week), macroscopic signs of photoaging were evaluated. Mice were then euthanized, and the skin was harvested for biochemical estimation of markers for oxidative stress, inflammation, matrix breakdown, and lysosomal function. Histopathological signs of photoaging were also evaluated with immunohistochemical detection of associated changes in autophagic and apoptotic markers. Metformin, mainly by topical application, improved clinical and histologic signs of photoaging. This was associated with suppression of the elevated oxidative stress, IL-6, matrix metalloproteinase 1, and caspase, with induction of cathepsin D and subsequent change in anti-LC3 and P62 staining in skin tissue. In addition to metformin antioxidant, anti-inflammatory, and antiapoptotic activities, its anti-photoaging effect is mainly attributed to enhancing autophagic flux by inducing cathepsin D. Its protective effect is boosted by coQ10, which supports their potential use in photoaging.
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         Rheumatology
         Gastroenterology
         Dermatology
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