Effects of Percutaneous Collagen Induction Therapy Associated with Hyaluronic Acid on Inflammatory Response, Oxidative Stress, and Collagen Production
Percutaneous collagen induction (PCI) is an alternative treatment for skin dysfunctions, it aims to stimulate collagen production by encouraging normal wound healing that occurs after any trauma by inducing microlesions; also it may be potentiated with the association with drugs such as hyaluronic a...
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Veröffentlicht in: | Inflammation 2020-12, Vol.43 (6), p.2232-2244 |
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creator | Corrêa, Maria Eduarda Anastácio Borges dos Santos Haupenthal, Daniela Pacheco Mendes, Carolini Zaccaron, Rubya Pereira de Roch Casagrande, Laura Venturini, Ligia Milanez Porto, Germano Duarte Bittencourt, João Vitor Silvano de Souza Silva, Jennyffer Ione de Sousa Mariano, Samara de Andrade, Thiago Antônio Moretti Silveira, Paulo Cesar Lock |
description | Percutaneous collagen induction (PCI) is an alternative treatment for skin dysfunctions, it aims to stimulate collagen production by encouraging normal wound healing that occurs after any trauma by inducing microlesions; also it may be potentiated with the association with drugs such as hyaluronic acid (HA). Our objective was to evaluate the effects of PCI associated with hyaluronic acid (0.9%) on inflammatory process, oxidative stress, and collagen production in rat epidermis. For the study, 36 adult Wistar rats were randomly divided into 6 groups (
n
= 6): Control; PCI 0.5; PCI 1.0; HA; PCI 0.5 + HA; and PCI 1.0 + HA. The animals were anesthetized, trichotomized, and the application of therapies was performed once; After 7 days, the animals were euthanized for removal of the skin region. Levels of pro-inflammatory (IL1, IL6, TNFα), anti-inflammatory (IL4 and IL10) cytokines and growth factors (FGF, TGFβ) were evaluated, besides oxidative stress parameters and histological analysis. In combination groups, there is a decrease in TNFα compared with the control and PCI groups in contrast to a significant increase in anti-inflammatory cytokines and growth factors. Oxidant and oxidative damage levels showed a significant decrease in PCI + HA groups in relation to PCI groups while antioxidant defense increased in PCI + HA groups compared with the control group. The number of fibroblasts was increased in the PCI 1.0 group in relation to the control, HA, and PCI 0.5. The number of blood vessels and collagen area was increased in groups PCI and PCI + HA compared with the HA group. We conclude that the combination of PCI with HA is able to accelerate the acute inflammatory process, reducing its deleterious effects and anticipating the chronic response, contributing to tissue repair. |
doi_str_mv | 10.1007/s10753-020-01291-0 |
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n
= 6): Control; PCI 0.5; PCI 1.0; HA; PCI 0.5 + HA; and PCI 1.0 + HA. The animals were anesthetized, trichotomized, and the application of therapies was performed once; After 7 days, the animals were euthanized for removal of the skin region. Levels of pro-inflammatory (IL1, IL6, TNFα), anti-inflammatory (IL4 and IL10) cytokines and growth factors (FGF, TGFβ) were evaluated, besides oxidative stress parameters and histological analysis. In combination groups, there is a decrease in TNFα compared with the control and PCI groups in contrast to a significant increase in anti-inflammatory cytokines and growth factors. Oxidant and oxidative damage levels showed a significant decrease in PCI + HA groups in relation to PCI groups while antioxidant defense increased in PCI + HA groups compared with the control group. The number of fibroblasts was increased in the PCI 1.0 group in relation to the control, HA, and PCI 0.5. The number of blood vessels and collagen area was increased in groups PCI and PCI + HA compared with the HA group. We conclude that the combination of PCI with HA is able to accelerate the acute inflammatory process, reducing its deleterious effects and anticipating the chronic response, contributing to tissue repair.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-020-01291-0</identifier><identifier>PMID: 32647956</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Antioxidants ; Antioxidants - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Blood vessels ; Collagen ; Collagen - metabolism ; Cytokines ; Cytokines - metabolism ; Epidermis ; Fibroblast growth factors ; Fibroblasts ; Fibroblasts - metabolism ; Growth factors ; Hyaluronic acid ; Hyaluronic Acid - metabolism ; Immunology ; Induction Chemotherapy ; Induction therapy ; Inflammation ; Interleukin 1 ; Interleukin 10 ; Interleukin 4 ; Interleukin 6 ; Internal Medicine ; Male ; Original Article ; Oxidants ; Oxidative Stress ; Pathology ; Percutaneous Coronary Intervention ; Pharmacology/Toxicology ; Rats ; Rats, Wistar ; Reactive Oxygen Species ; Rheumatology ; Tissue engineering ; Trauma ; Tumor necrosis factor-α ; Wound healing ; Wound Healing - drug effects</subject><ispartof>Inflammation, 2020-12, Vol.43 (6), p.2232-2244</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-9482c1375ef59be18275b7cf19afc548ccf6d4f874a12bee5d267132659285df3</citedby><cites>FETCH-LOGICAL-c375t-9482c1375ef59be18275b7cf19afc548ccf6d4f874a12bee5d267132659285df3</cites><orcidid>0000-0003-4908-2257</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-020-01291-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-020-01291-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32647956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Corrêa, Maria Eduarda Anastácio Borges</creatorcontrib><creatorcontrib>dos Santos Haupenthal, Daniela Pacheco</creatorcontrib><creatorcontrib>Mendes, Carolini</creatorcontrib><creatorcontrib>Zaccaron, Rubya Pereira</creatorcontrib><creatorcontrib>de Roch Casagrande, Laura</creatorcontrib><creatorcontrib>Venturini, Ligia Milanez</creatorcontrib><creatorcontrib>Porto, Germano Duarte</creatorcontrib><creatorcontrib>Bittencourt, João Vitor Silvano</creatorcontrib><creatorcontrib>de Souza Silva, Jennyffer Ione</creatorcontrib><creatorcontrib>de Sousa Mariano, Samara</creatorcontrib><creatorcontrib>de Andrade, Thiago Antônio Moretti</creatorcontrib><creatorcontrib>Silveira, Paulo Cesar Lock</creatorcontrib><title>Effects of Percutaneous Collagen Induction Therapy Associated with Hyaluronic Acid on Inflammatory Response, Oxidative Stress, and Collagen Production</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Percutaneous collagen induction (PCI) is an alternative treatment for skin dysfunctions, it aims to stimulate collagen production by encouraging normal wound healing that occurs after any trauma by inducing microlesions; also it may be potentiated with the association with drugs such as hyaluronic acid (HA). Our objective was to evaluate the effects of PCI associated with hyaluronic acid (0.9%) on inflammatory process, oxidative stress, and collagen production in rat epidermis. For the study, 36 adult Wistar rats were randomly divided into 6 groups (
n
= 6): Control; PCI 0.5; PCI 1.0; HA; PCI 0.5 + HA; and PCI 1.0 + HA. The animals were anesthetized, trichotomized, and the application of therapies was performed once; After 7 days, the animals were euthanized for removal of the skin region. Levels of pro-inflammatory (IL1, IL6, TNFα), anti-inflammatory (IL4 and IL10) cytokines and growth factors (FGF, TGFβ) were evaluated, besides oxidative stress parameters and histological analysis. In combination groups, there is a decrease in TNFα compared with the control and PCI groups in contrast to a significant increase in anti-inflammatory cytokines and growth factors. Oxidant and oxidative damage levels showed a significant decrease in PCI + HA groups in relation to PCI groups while antioxidant defense increased in PCI + HA groups compared with the control group. The number of fibroblasts was increased in the PCI 1.0 group in relation to the control, HA, and PCI 0.5. The number of blood vessels and collagen area was increased in groups PCI and PCI + HA compared with the HA group. We conclude that the combination of PCI with HA is able to accelerate the acute inflammatory process, reducing its deleterious effects and anticipating the chronic response, contributing to tissue repair.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood vessels</subject><subject>Collagen</subject><subject>Collagen - metabolism</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Epidermis</subject><subject>Fibroblast growth factors</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Growth factors</subject><subject>Hyaluronic acid</subject><subject>Hyaluronic Acid - metabolism</subject><subject>Immunology</subject><subject>Induction Chemotherapy</subject><subject>Induction therapy</subject><subject>Inflammation</subject><subject>Interleukin 1</subject><subject>Interleukin 10</subject><subject>Interleukin 4</subject><subject>Interleukin 6</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Original Article</subject><subject>Oxidants</subject><subject>Oxidative Stress</subject><subject>Pathology</subject><subject>Percutaneous Coronary Intervention</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species</subject><subject>Rheumatology</subject><subject>Tissue engineering</subject><subject>Trauma</subject><subject>Tumor necrosis factor-α</subject><subject>Wound healing</subject><subject>Wound Healing - 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metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood vessels</topic><topic>Collagen</topic><topic>Collagen - metabolism</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Epidermis</topic><topic>Fibroblast growth factors</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Growth factors</topic><topic>Hyaluronic acid</topic><topic>Hyaluronic Acid - metabolism</topic><topic>Immunology</topic><topic>Induction Chemotherapy</topic><topic>Induction therapy</topic><topic>Inflammation</topic><topic>Interleukin 1</topic><topic>Interleukin 10</topic><topic>Interleukin 4</topic><topic>Interleukin 6</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Original Article</topic><topic>Oxidants</topic><topic>Oxidative Stress</topic><topic>Pathology</topic><topic>Percutaneous Coronary Intervention</topic><topic>Pharmacology/Toxicology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species</topic><topic>Rheumatology</topic><topic>Tissue engineering</topic><topic>Trauma</topic><topic>Tumor necrosis factor-α</topic><topic>Wound healing</topic><topic>Wound Healing - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Corrêa, Maria Eduarda Anastácio Borges</creatorcontrib><creatorcontrib>dos Santos Haupenthal, Daniela Pacheco</creatorcontrib><creatorcontrib>Mendes, Carolini</creatorcontrib><creatorcontrib>Zaccaron, Rubya Pereira</creatorcontrib><creatorcontrib>de Roch Casagrande, Laura</creatorcontrib><creatorcontrib>Venturini, Ligia Milanez</creatorcontrib><creatorcontrib>Porto, Germano Duarte</creatorcontrib><creatorcontrib>Bittencourt, João Vitor Silvano</creatorcontrib><creatorcontrib>de Souza Silva, Jennyffer Ione</creatorcontrib><creatorcontrib>de Sousa Mariano, Samara</creatorcontrib><creatorcontrib>de Andrade, Thiago Antônio Moretti</creatorcontrib><creatorcontrib>Silveira, Paulo Cesar Lock</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Corrêa, Maria Eduarda Anastácio Borges</au><au>dos Santos Haupenthal, Daniela Pacheco</au><au>Mendes, Carolini</au><au>Zaccaron, Rubya Pereira</au><au>de Roch Casagrande, Laura</au><au>Venturini, Ligia Milanez</au><au>Porto, Germano Duarte</au><au>Bittencourt, João Vitor Silvano</au><au>de Souza Silva, Jennyffer Ione</au><au>de Sousa Mariano, Samara</au><au>de Andrade, Thiago Antônio Moretti</au><au>Silveira, Paulo Cesar Lock</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Percutaneous Collagen Induction Therapy Associated with Hyaluronic Acid on Inflammatory Response, Oxidative Stress, and Collagen Production</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>43</volume><issue>6</issue><spage>2232</spage><epage>2244</epage><pages>2232-2244</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Percutaneous collagen induction (PCI) is an alternative treatment for skin dysfunctions, it aims to stimulate collagen production by encouraging normal wound healing that occurs after any trauma by inducing microlesions; also it may be potentiated with the association with drugs such as hyaluronic acid (HA). Our objective was to evaluate the effects of PCI associated with hyaluronic acid (0.9%) on inflammatory process, oxidative stress, and collagen production in rat epidermis. For the study, 36 adult Wistar rats were randomly divided into 6 groups (
n
= 6): Control; PCI 0.5; PCI 1.0; HA; PCI 0.5 + HA; and PCI 1.0 + HA. The animals were anesthetized, trichotomized, and the application of therapies was performed once; After 7 days, the animals were euthanized for removal of the skin region. Levels of pro-inflammatory (IL1, IL6, TNFα), anti-inflammatory (IL4 and IL10) cytokines and growth factors (FGF, TGFβ) were evaluated, besides oxidative stress parameters and histological analysis. In combination groups, there is a decrease in TNFα compared with the control and PCI groups in contrast to a significant increase in anti-inflammatory cytokines and growth factors. Oxidant and oxidative damage levels showed a significant decrease in PCI + HA groups in relation to PCI groups while antioxidant defense increased in PCI + HA groups compared with the control group. The number of fibroblasts was increased in the PCI 1.0 group in relation to the control, HA, and PCI 0.5. The number of blood vessels and collagen area was increased in groups PCI and PCI + HA compared with the HA group. We conclude that the combination of PCI with HA is able to accelerate the acute inflammatory process, reducing its deleterious effects and anticipating the chronic response, contributing to tissue repair.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32647956</pmid><doi>10.1007/s10753-020-01291-0</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-4908-2257</orcidid></addata></record> |
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subjects | Animals Antioxidants Antioxidants - metabolism Biomedical and Life Sciences Biomedicine Blood vessels Collagen Collagen - metabolism Cytokines Cytokines - metabolism Epidermis Fibroblast growth factors Fibroblasts Fibroblasts - metabolism Growth factors Hyaluronic acid Hyaluronic Acid - metabolism Immunology Induction Chemotherapy Induction therapy Inflammation Interleukin 1 Interleukin 10 Interleukin 4 Interleukin 6 Internal Medicine Male Original Article Oxidants Oxidative Stress Pathology Percutaneous Coronary Intervention Pharmacology/Toxicology Rats Rats, Wistar Reactive Oxygen Species Rheumatology Tissue engineering Trauma Tumor necrosis factor-α Wound healing Wound Healing - drug effects |
title | Effects of Percutaneous Collagen Induction Therapy Associated with Hyaluronic Acid on Inflammatory Response, Oxidative Stress, and Collagen Production |
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