A Molecular Perspective on the Potential Benefits of Metformin for the Treatment of Inflammatory Skin Disorders

Chang, Ji‐Eun; Choi, Min Sik

doi:10.3390/ijms21238960

Cited by 24 publications

(23 citation statements)

References 96 publications

(112 reference statements)

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“…Our present results indicated that metformin treatment significantly increased the plasma concentration of the indices of the oxidative stress and reduced the pro-inflammatory mediators. These actions support the reports that metformin is a strong antioxidant and anti-inflammatory agent [22,45].…”

Section: Discussionsupporting

confidence: 89%

“…Metformin has also been reported to prevent fibrosis in several organs, including the kidneys [18,19]. In addition to treatment of diabetes, the drug has also been reported to be beneficial in treating several other diseases and conditions that include lung and breast cancers [20,21], inflammatory skin disorders [22], and neurological diseases [23].…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Metformin in Diabetic and Non-Diabetic Rats with Experimentally-Induced Chronic Kidney Disease

et al. 2021

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This work aimed to investigate whether treatment with the antidiabetic drug metformin would affect adenine-induced chronic kidney disease (CKD) in non-diabetic rats and rats with streptozotocin (STZ)-induced diabetes. Rats were randomly divided into eight groups, and given either normal feed, or feed mixed with adenine (0.25% w/w, for five weeks) to induce CKD. Some of these groups were also simultaneously treated orally with metformin (200 mg/kg/day). Rats given adenine showed the typical signs of CKD that included detrimental changes in several physiological and traditional and novel biochemical biomarkers in plasma urine and kidney homogenates such as albumin/creatinine ratio, N-acetyl-beta-D-glucosaminidase, neutrophil gelatinase-associated lipocalin, 8-isoprostane, adiponectin, cystatin C, as well as plasma urea, creatinine, uric acid, indoxyl sulfate, calcium, and phosphorus. Several indices of inflammation and oxidative stress, and renal nuclear factor-κB and nuclear factor erythroid 2-related factor 2 levels were also measured. Histopathologically, adenine caused renal tubular necrosis and fibrosis. The activation of the intracellular mitogen-activated protein kinase signaling pathway was inhibited in the groups that received metformin and STZ together, with or without adenine induced-CKD. Induction of diabetes worsened most of the actions induced by adenine. Metformin significantly ameliorated the renal actions induced by adenine and STZ when these were given singly, and more so when given together. The results suggest that metformin can be a useful drug in attenuating the progression of CKD in both diabetic and non-diabetic rats.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

The Effect of Metformin in Diabetic and Non-Diabetic Rats with Experimentally-Induced Chronic Kidney Disease

et al. 2021

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“…In addition to its role in psoriasis, metformin may play an essential role in several dermatological conditions such as acanthosis nigricans, acne, disorders of increased pigmentation, allergic contact dermatitis, eruptive xanthomas, suppurative hidradenitis, hirsutism, squamous cell carcinoma, and melanoma [ 54 , 55 , 56 ]. Several antidiabetic drugs have been studied for their effect on psoriasis ( Table 4 ).…”

Section: Resultsmentioning

confidence: 99%

Is Metformin a Possible Beneficial Treatment for Psoriasis? A Scoping Review

Stănescu

Simionescu

Florea

et al. 2021

JPM

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Psoriasis is a chronic inflammatory condition with genetic, immunological, and metabolic etiology. The link between psoriasis and diabetes mellitus has been shown in genetic predisposition, environmental influences, inflammatory pathways, and insulin resistance, resulting in end-organ damage in both conditions. Because comorbidities often accompany psoriasis, the therapeutic management of the disease must also take into consideration the comorbidities. Given that metformin’s therapeutic role in psoriasis is not yet fully elucidated, we raised the question of whether metformin is a viable alternative for the treatment of psoriasis. We conducted this scoping review by searching for evidence in PubMed, Cochrane, and Scopus databases, and we used an extension for scoping reviews (PRISMA-ScR). Current evidence suggests that metformin is safe to use in psoriasis. Studies have shown an excellent therapeutic response to metformin in patients with psoriasis and comorbidities such as diabetes, metabolic syndrome, and obesity. There is no clear evidence supporting metformin monotherapy in patients with psoriasis without comorbidities. There is a need to further evaluate metformin in larger clinical trials, as a therapy in psoriasis.

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“…Metformin is utilized as a rst-line antidiabetic agent for the treatment of type 2 diabetes mellitus (T2DM), as it has been shown to improve metabolic homeostasis including hyperglycemia and dyslipidemia. Previous studies have demonstrated that the long-term use of metformin is associated with a reduced risk of psoriasis [14,15]. However, further studies are required to identify the potential mechanism.…”

Section: Forkhead Box O 3 (Foxo3mentioning

confidence: 99%

Metformin prevents the psoriasis under hyperlipidemia via activation of the FOXO3

Zhang

Liu

et al. 2022

Preprint

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Background: Psoriasis patients have obvious lipid metabolism disorders. The hyperlipidemia aggravates the development of psoriasis. In this study, we investigated that under the hyperlipidemia conditions, whether metformin could alleviate psoriasis via a Forkhead box O 3 (FOXO3)-driven pathway, as well as the mechanisms underlying. Methods: Wild type or FOXO3 knockdown HaCat cells were treated with free fatty acids (FFA) for 10 days and then co-treated with metformin for another 4 days. Triglyceride (TG) level, cell viability, proliferation, apoptosis, antioxidant enzymes, ROS levels, as well as the transcription activity of FOXO3 were analyzed. Results: Our data showed that FFA treatment promoted the proliferation and inhibited the apoptosis in HaCat cells. However, metformin could reversed all of these changes. Metformin treatment significantly increased the expressions and the activities of superoxide dismutase (SOD) and catalase (CAT), and reduced the reactive oxygen species (ROS) level, while FFA inhibited the antioxidant enzymes and increased the ROS level in HaCat cells. Metformin significantly promoted the autophagy and increase FOXO3 protein level in the nucleus under hyperlipidemia conditions, which was significantly inhibited by FFA treatment. However, all of the effects from metformin were partially blocked by FOXO3 knockdown. Conclusion: This study demonstrated that under the hyperlipidemia conditions, metformin has significant antiproliferation and proapoptosis effects by reducing ROS level as well as increasing autophagy. Both of these were responsible for the alleviation of psoriasis. All of these effects from metformin were through FOXO3-dependent pathway.

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A Molecular Perspective on the Potential Benefits of Metformin for the Treatment of Inflammatory Skin Disorders

Cited by 24 publications

References 96 publications

The Effect of Metformin in Diabetic and Non-Diabetic Rats with Experimentally-Induced Chronic Kidney Disease

The Effect of Metformin in Diabetic and Non-Diabetic Rats with Experimentally-Induced Chronic Kidney Disease

Is Metformin a Possible Beneficial Treatment for Psoriasis? A Scoping Review

Metformin prevents the psoriasis under hyperlipidemia via activation of the FOXO3

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