Buffalo casein derived peptide can alleviates H 2 O 2 induced cellular damage and necrosis in fibroblast cells

Devi, Savita; Kumar, Naveen; Kapila, Suman; Mada, Sanusi Bello; Reddi, Srinu; Vij, Rishika; Kapila, Rajeev

doi:10.1016/j.etp.2017.04.009

Cited by 29 publications

(12 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For instance, P53 induces glutathione peroxidase (GPX) activity, which is an enzyme for H 2 O 2 conversion to H 2 O and O 2 by using GSH as a coenzyme [28,31]. Our study showed that AME reduced the SOD activity and increased the GSH levels after 48 h, which reinforces the protective effect of AME on oxidative stressinduced ageing cells, by suppressing the antioxidant system in agreement with a similar study on rat fibroblasts [32]. Moreover, in compliance with the antioxidants analysis results, the P53 and P21 expression was assessed after 48 h of pre-and post-treatment of AME; and, as we discussed before, AME diminished the P53 expression; so, it reduced the GPX activation and as we expected, GSH consumption confirms the elevation of GSH levels.…”

Section: Discussionsupporting

confidence: 90%

Protective effect of human amniotic membrane extract against hydrogen peroxide‐induced oxidative damage in human dermal fibroblasts

Talachi

Afzal

Nouri

et al. 2022

Intern J of Cosmetic Sci

View full text Add to dashboard Cite

Objective One of the main approaches to preventing skin ageing is to protect fibroblast cells from oxidative stress. The promoting effect of the human amniotic membrane extract (hAME) on re‐epithelization, proliferation and migration of cells in wound healing has been already well studied. This experimental study aimed to investigate the antioxidant activity of hAME against hydrogen peroxide (H2O2)‐induced dermal fibroblast damage. Methods Here, to establish the ageing model, human foreskin fibroblasts (HFFs) were exposed to 200 μM H2O2 for 2 h. HFFs were treated with 0.1 mg/ml AME for 24 or 48 h before or/and after H2O2 exposure. A total of 48 h following the H2O2 treatment, we measured cell proliferation, viability, senescence‐associated β‐galactosidase (SA‐β‐Gal), antioxidants and preinflammatory cytokine (IL‐6) levels, as well as the expression of senescence‐associated genes (P53 and P21). Results The obtained results indicated that under oxidative stress, AME significantly increased cellular viability and not only promoted the cell proliferation rate but also attenuated apoptotic induction condition (p < 0.001). AME also significantly reversed the SA‐β‐Gal levels induced by H2O2 (p < 0.001). Additionally, both pre‐ and post‐treatment regimen by AME down‐regulated the expression of senescence marker genes (p < 0.001). Moreover, AME declined different oxidative stress biomarkers such as superoxide dismutase and catalase and increased the glutathione amount. Conclusion Altogether, our results indicated that AME had a remarkable antioxidant and antiageing activity as pre‐ and post‐treatment regimen, pointing to this compound as a potential natural‐based cosmeceutical agent to prevent and treat skin ageing conditions.

show abstract

Section: Discussionsupporting

confidence: 90%

Protective effect of human amniotic membrane extract against hydrogen peroxide‐induced oxidative damage in human dermal fibroblasts

Talachi

Afzal

Nouri

et al. 2022

Intern J of Cosmetic Sci

View full text Add to dashboard Cite

show abstract

“…In this regard, both BPH-19 and FBPH-3 manage to re-establish the cell cycle at the control level (figure 5 In line with these results, other authors have reported that pre-treatment with peptides from krill protein hydrolysates can prevent subG1 phase accumulation in H2O2stimulated cells (Fernando et al 2020). (Devi et al 2017). There are few studies that analyze the ability of hydrolysates with cytoprotective effect to prevent cell death by different pathways.…”

Section: Cell Cyclesupporting

confidence: 67%

Segurança alimentar e nutricional 4

Castro¹

2023

View full text Add to dashboard Cite

Os autores desta obra: 1. Atestam não possuir qualquer interesse comercial que constitua um conflito de interesses em relação ao artigo científico publicado; 2.Declaram que participaram ativamente da construção dos respectivos manuscritos, preferencialmente na: a) Concepção do estudo, e/ou aquisição de dados, e/ou análise e interpretação de dados; b) Elaboração do artigo ou revisão com vistas a tornar o material intelectualmente relevante; c) Aprovação final do manuscrito para submissão.; 3. Certificam que os artigos científicos publicados estão completamente isentos de dados e/ou resultados fraudulentos; 4. Confirmam a citação e a referência correta de todos os dados e de interpretações de dados de outras pesquisas; 5.Reconhecem terem informado todas as fontes de financiamento recebidas para a consecução da pesquisa; 6. Autorizam a edição da obra, que incluem os registros de ficha catalográfica, ISBN, DOI e demais indexadores, projeto visual e criação de capa, diagramação de miolo, assim como lançamento e divulgação da mesma conforme critérios da Atena Editora. DECLARAÇÃO DA EDITORA A Atena Editora declara, para os devidos fins de direito, que: 1. A presente publicação constitui apenas transferência temporária dos direitos autorais, direito sobre a publicação, inclusive não constitui responsabilidade solidária na criação dos manuscritos publicados, nos termos previstos na Lei sobre direitos autorais (Lei 9610/98), no art. 184 do Código Penal e no art. 927 do Código Civil; 2. Autoriza e incentiva os autores a assinarem contratos com repositórios institucionais, com fins exclusivos de divulgação da obra, desde que com o devido reconhecimento de autoria e edição e sem qualquer finalidade comercial; 3. Todos os e-book são open access, desta forma não os comercializa em seu site, sites parceiros, plataformas de ecommerce, ou qualquer outro meio virtual ou físico, portanto, está isenta de repasses de direitos autorais aos autores; 4. Todos os membros do conselho editorial são doutores e vinculados a instituições de ensino superior públicas, conforme recomendação da CAPES para obtenção do Qualis livro; 5. Não cede, comercializa ou autoriza a utilização dos nomes e e-mails dos autores, bem como nenhum outro dado dos mesmos, para qualquer finalidade que não o escopo da divulgação desta obra.

show abstract

“…TIMP-2 and TIMP-1 can non-covalently bind with MMP-2 and MMP-9, respectively, to prevent direct damage to the ECM caused by the transformation process from proenzyme to active enzyme [47]. As the expression of TIMP-1 and TIMP-2 decreases, the balance between MMPs and TIMPs is disrupted, which weakens the inhibitory effects of TIMPs on MMPs and causes the secretion of a large amount of MMPs, resulting in skin damage and even pathological changes [48]. In this study, KTP increased TIMP-1 and TIMP-2 expression and decreased MMP-2 and MMP-9 expression in mice with skin damage.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Kuding Tea (Ilex kudingcha C. J. Tseng) Polyphenols on UVB-Induced Skin Aging in SKH1 Hairless Mice

Zhang²,

Sun

et al. 2019

Molecules

View full text Add to dashboard Cite

In this study, the protective effects of Kuding tea polyphenols (KTPs) on ultraviolet B (UVB)-induced skin injury of SKH1 hairless mice were studied. The ion precipitation method was used for extraction of polyphenols from Kuding tea. High-performance liquid chromatography showed that KTPs contains chlorogenic acid, cryptochlorogenic acid, isochlorogenic acid B, isochlorogenic acid A, and isochlorogenic acid C. SKH1 hairless mice were induced skin aging using 2.0 mW/s intensity of 90 mJ/cm2 UV light once a day for seven weeks. The 2.5% and 5% KTPs solution was smeared on 2 cm2 of back skin of skin aging mice twice a day. Mouse experiments showed that KTP strongly increased the serum levels of total superoxide dismutase (T-SOD) and catalase (CAT) and reduced those of malondialdehyde, interleukin 6 (IL-6), IL-1β, and tumor necrosis factor alpha (TNF-α) in mice with UVB-induced skin damage. KTP also increased the levels of type 1 collagen (Col I), hydroxyproline, and hyaluronic acid and reduced those of Col III and hydrogen peroxide in the damaged skin tissues of mice. Pathological observations of tissues stained with H & E, Masson’s trichrome, Verhoeff, and toluidine blue showed that KTPs could protect skin cells, collagen, and elastin and decrease the number of mast cells, thus inhibiting skin damage. Quantitative PCR and western blot assays showed that KTP upregulated the mRNA and protein expression of tissue inhibitor of metalloproteinase 1 (TIMP-1), TIMP-2, copper/zinc-SOD, manganese-SOD, CAT, and glutathione peroxidase and downregulated the expression of matrix metalloproteinase 2 (MMP-2) and MMP-9. In addition, the same concentration of KTP had stronger protective effects than vitamin C. The results of this study demonstrate that KTPs have good skin protective effects, as they are able to inhibit UVB-induced skin damage.

show abstract

Buffalo casein derived peptide can alleviates H 2 O 2 induced cellular damage and necrosis in fibroblast cells

Cited by 29 publications

References 38 publications

Protective effect of human amniotic membrane extract against hydrogen peroxide‐induced oxidative damage in human dermal fibroblasts

Protective effect of human amniotic membrane extract against hydrogen peroxide‐induced oxidative damage in human dermal fibroblasts

Segurança alimentar e nutricional 4

Protective Effects of Kuding Tea (Ilex kudingcha C. J. Tseng) Polyphenols on UVB-Induced Skin Aging in SKH1 Hairless Mice

Contact Info

Product

Resources

About