Attenuation of inflammation, oxidative stress and TGF-β1/Smad3 signaling and upregulation of Nrf2/HO-1 signaling mediate the protective effect of diallyl disulfide against cadmium nephrotoxicity
Heavy metals are toxic environmental pollutants with serious health effects on humans and animals. Cadmium (Cd) is known for its serious nephrotoxic effect and its toxicity involves oxidative stress (OS) and inflammation. Diallyl disulfide (DADS), a main constituent of garlic, exhibites cytoprotecti...
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| creator | Alruhaimi, Reem S. Hassanein, Emad H.M. Ahmeda, Ahmad F. Alnasser, Sulaiman M. Atwa, Ahmed M. Sabry, Mostafa Alzoghaibi, Mohammed A. Mahmoud, Ayman M. |
| description | Heavy metals are toxic environmental pollutants with serious health effects on humans and animals. Cadmium (Cd) is known for its serious nephrotoxic effect and its toxicity involves oxidative stress (OS) and inflammation. Diallyl disulfide (DADS), a main constituent of garlic, exhibites cytoprotective and antioxidant activities. This study investigated the effect of DADS on OS, inflammation, and fibrosis induced by Cd in rat kidney, pointing to the involvement of transforming growth factor-β (TGF-β)/Smad3 and nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, and peroxisome proliferator-activated receptor gamma (PPARγ). Rats received DADS for 14 days and Cd on day 7 and blood and kidney samples were collected. Cd elevated serum creatinine, urea and uric acid, provoked kidney histopathological alterations and collagen deposition, increased kidney malondialdehyde (MDA) level, and decreased glutathione (GSH) and antioxidant enzymes. Nuclear factor-kappaB (NF-κB) p65, interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1β, and CD68 were upregulated in Cd-administered rat kidney. DADS prevented kidney injury, mitigated OS, suppressed NF-κB, CD68 and pro-inflammatory mediators, and boosted antioxidants. DADS downregulated TGF-β1, Smad3 phosphorylation and Kelch-like ECH-associated protein-1 (Keap1), and increased Nrf2, HO-1, cytoglobin, and PPARγ. In conclusion, DADS protects the kidney against Cd toxicity by attenuating OS, inflammation, and TGF-β1/Smad3 signaling, and enhancement of Nrf2/HO-1 signaling, antioxidants, and PPARγ.
•Cadmium induces oxidative stress, inflammation and fibrosis in rat kidney.•Diallyl disulfide prevents cadmium-induced nephrotoxicity.•Diallyl disulfide mitigates cadmium-induced oxidative stress and inflammation.•Diallyl disulfide downregulates TGF-β1/Smad3 and upregulated Nrf2/HO-1 signaling. |
| doi_str_mv | 10.1016/j.tice.2024.102576 |
| format | Article |
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•Cadmium induces oxidative stress, inflammation and fibrosis in rat kidney.•Diallyl disulfide prevents cadmium-induced nephrotoxicity.•Diallyl disulfide mitigates cadmium-induced oxidative stress and inflammation.•Diallyl disulfide downregulates TGF-β1/Smad3 and upregulated Nrf2/HO-1 signaling.</description><identifier>ISSN: 0040-8166</identifier><identifier>ISSN: 1532-3072</identifier><identifier>EISSN: 1532-3072</identifier><identifier>DOI: 10.1016/j.tice.2024.102576</identifier><identifier>PMID: 39353227</identifier><language>eng</language><publisher>Scotland: Elsevier Ltd</publisher><subject>Allyl Compounds - pharmacology ; Animals ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Cadmium ; Cadmium - toxicity ; Disulfides - pharmacology ; Garlic ; Heavy metals ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Inflammation - pathology ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - chemically induced ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidney Diseases - prevention & control ; Male ; Nephrotoxicity ; NF-E2-Related Factor 2 - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; PPAR gamma - metabolism ; Protective Agents - pharmacology ; Rats ; Rats, Wistar ; Signal Transduction - drug effects ; Smad3 Protein - metabolism ; Transforming Growth Factor beta1 - metabolism ; Up-Regulation - drug effects</subject><ispartof>Tissue & cell, 2024-12, Vol.91, p.102576, Article 102576</ispartof><rights>2024 Elsevier Ltd</rights><rights>Copyright © 2024 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c237t-e344f5d978ff4b0a3ea9bb7d78b91a3cd4f57c6b5b6cc2bc924c0aa0d6b4ff343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0040816624002775$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39353227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alruhaimi, Reem S.</creatorcontrib><creatorcontrib>Hassanein, Emad H.M.</creatorcontrib><creatorcontrib>Ahmeda, Ahmad F.</creatorcontrib><creatorcontrib>Alnasser, Sulaiman M.</creatorcontrib><creatorcontrib>Atwa, Ahmed M.</creatorcontrib><creatorcontrib>Sabry, Mostafa</creatorcontrib><creatorcontrib>Alzoghaibi, Mohammed A.</creatorcontrib><creatorcontrib>Mahmoud, Ayman M.</creatorcontrib><title>Attenuation of inflammation, oxidative stress and TGF-β1/Smad3 signaling and upregulation of Nrf2/HO-1 signaling mediate the protective effect of diallyl disulfide against cadmium nephrotoxicity</title><title>Tissue & cell</title><addtitle>Tissue Cell</addtitle><description>Heavy metals are toxic environmental pollutants with serious health effects on humans and animals. Cadmium (Cd) is known for its serious nephrotoxic effect and its toxicity involves oxidative stress (OS) and inflammation. Diallyl disulfide (DADS), a main constituent of garlic, exhibites cytoprotective and antioxidant activities. This study investigated the effect of DADS on OS, inflammation, and fibrosis induced by Cd in rat kidney, pointing to the involvement of transforming growth factor-β (TGF-β)/Smad3 and nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, and peroxisome proliferator-activated receptor gamma (PPARγ). Rats received DADS for 14 days and Cd on day 7 and blood and kidney samples were collected. Cd elevated serum creatinine, urea and uric acid, provoked kidney histopathological alterations and collagen deposition, increased kidney malondialdehyde (MDA) level, and decreased glutathione (GSH) and antioxidant enzymes. Nuclear factor-kappaB (NF-κB) p65, interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1β, and CD68 were upregulated in Cd-administered rat kidney. DADS prevented kidney injury, mitigated OS, suppressed NF-κB, CD68 and pro-inflammatory mediators, and boosted antioxidants. DADS downregulated TGF-β1, Smad3 phosphorylation and Kelch-like ECH-associated protein-1 (Keap1), and increased Nrf2, HO-1, cytoglobin, and PPARγ. In conclusion, DADS protects the kidney against Cd toxicity by attenuating OS, inflammation, and TGF-β1/Smad3 signaling, and enhancement of Nrf2/HO-1 signaling, antioxidants, and PPARγ.
•Cadmium induces oxidative stress, inflammation and fibrosis in rat kidney.•Diallyl disulfide prevents cadmium-induced nephrotoxicity.•Diallyl disulfide mitigates cadmium-induced oxidative stress and inflammation.•Diallyl disulfide downregulates TGF-β1/Smad3 and upregulated Nrf2/HO-1 signaling.</description><subject>Allyl Compounds - pharmacology</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Cadmium</subject><subject>Cadmium - toxicity</subject><subject>Disulfides - pharmacology</subject><subject>Garlic</subject><subject>Heavy metals</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - prevention & control</subject><subject>Male</subject><subject>Nephrotoxicity</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>PPAR gamma - metabolism</subject><subject>Protective Agents - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Signal Transduction - drug effects</subject><subject>Smad3 Protein - metabolism</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Up-Regulation - drug effects</subject><issn>0040-8166</issn><issn>1532-3072</issn><issn>1532-3072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9Uc1OGzEQtlArCLQv0EPlYw_dxD-766zUC0IFKqFyAM6W1x4HR15vantR81p9hd77TDgJRT31NGN_Px7Ph9AHSuaU0HaxnmenYc4Iq8sFa0R7hGa04aziRLA3aEZITaolbdsTdJrSmhAiaiqO0QnveKExMUO_z3OGMKnsxoBHi12wXg3D_vwZjz-dKe0T4JQjpIRVMPj-6rL684su7gZlOE5uFZR3YbXHpk2E1eRf7b5HyxbXtxX9hzeAcSoDzo-AN3HMoPcvgLWl24kK7P3Wl5omb50BrFbKhZSxVmZw04ADbB6LsoynXd6-Q2-t8gnev9Qz9HD59f7iurq5vfp2cX5TacZFroDXtW1MJ5bW1j1RHFTX98KIZd9RxbUpqNBt3_St1qzXHas1UYqYtq-t5TU_Q58OvmXqHxOkLAeXNHivAoxTkpxS1lC2bGmhsgNVxzGlCFZuohtU3EpK5C48uZa78OQuPHkIr4g-vvhPfVnSq-RvWoXw5UCA8ssnB1Em7SDostBYdifN6P7n_wxibrDR</recordid><startdate>202412</startdate><enddate>202412</enddate><creator>Alruhaimi, Reem S.</creator><creator>Hassanein, Emad H.M.</creator><creator>Ahmeda, Ahmad F.</creator><creator>Alnasser, Sulaiman M.</creator><creator>Atwa, Ahmed M.</creator><creator>Sabry, Mostafa</creator><creator>Alzoghaibi, Mohammed A.</creator><creator>Mahmoud, Ayman M.</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202412</creationdate><title>Attenuation of inflammation, oxidative stress and TGF-β1/Smad3 signaling and upregulation of Nrf2/HO-1 signaling mediate the protective effect of diallyl disulfide against cadmium nephrotoxicity</title><author>Alruhaimi, Reem S. ; Hassanein, Emad H.M. ; Ahmeda, Ahmad F. ; Alnasser, Sulaiman M. ; Atwa, Ahmed M. ; Sabry, Mostafa ; Alzoghaibi, Mohammed A. ; Mahmoud, Ayman M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c237t-e344f5d978ff4b0a3ea9bb7d78b91a3cd4f57c6b5b6cc2bc924c0aa0d6b4ff343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Allyl Compounds - pharmacology</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Antioxidants - pharmacology</topic><topic>Cadmium</topic><topic>Cadmium - toxicity</topic><topic>Disulfides - pharmacology</topic><topic>Garlic</topic><topic>Heavy metals</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - prevention & control</topic><topic>Male</topic><topic>Nephrotoxicity</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>PPAR gamma - metabolism</topic><topic>Protective Agents - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Signal Transduction - drug effects</topic><topic>Smad3 Protein - metabolism</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alruhaimi, Reem S.</creatorcontrib><creatorcontrib>Hassanein, Emad H.M.</creatorcontrib><creatorcontrib>Ahmeda, Ahmad F.</creatorcontrib><creatorcontrib>Alnasser, Sulaiman M.</creatorcontrib><creatorcontrib>Atwa, Ahmed M.</creatorcontrib><creatorcontrib>Sabry, Mostafa</creatorcontrib><creatorcontrib>Alzoghaibi, Mohammed A.</creatorcontrib><creatorcontrib>Mahmoud, Ayman M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Tissue & cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alruhaimi, Reem S.</au><au>Hassanein, Emad H.M.</au><au>Ahmeda, Ahmad F.</au><au>Alnasser, Sulaiman M.</au><au>Atwa, Ahmed M.</au><au>Sabry, Mostafa</au><au>Alzoghaibi, Mohammed A.</au><au>Mahmoud, Ayman M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attenuation of inflammation, oxidative stress and TGF-β1/Smad3 signaling and upregulation of Nrf2/HO-1 signaling mediate the protective effect of diallyl disulfide against cadmium nephrotoxicity</atitle><jtitle>Tissue & cell</jtitle><addtitle>Tissue Cell</addtitle><date>2024-12</date><risdate>2024</risdate><volume>91</volume><spage>102576</spage><pages>102576-</pages><artnum>102576</artnum><issn>0040-8166</issn><issn>1532-3072</issn><eissn>1532-3072</eissn><abstract>Heavy metals are toxic environmental pollutants with serious health effects on humans and animals. Cadmium (Cd) is known for its serious nephrotoxic effect and its toxicity involves oxidative stress (OS) and inflammation. Diallyl disulfide (DADS), a main constituent of garlic, exhibites cytoprotective and antioxidant activities. This study investigated the effect of DADS on OS, inflammation, and fibrosis induced by Cd in rat kidney, pointing to the involvement of transforming growth factor-β (TGF-β)/Smad3 and nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, and peroxisome proliferator-activated receptor gamma (PPARγ). Rats received DADS for 14 days and Cd on day 7 and blood and kidney samples were collected. Cd elevated serum creatinine, urea and uric acid, provoked kidney histopathological alterations and collagen deposition, increased kidney malondialdehyde (MDA) level, and decreased glutathione (GSH) and antioxidant enzymes. Nuclear factor-kappaB (NF-κB) p65, interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1β, and CD68 were upregulated in Cd-administered rat kidney. DADS prevented kidney injury, mitigated OS, suppressed NF-κB, CD68 and pro-inflammatory mediators, and boosted antioxidants. DADS downregulated TGF-β1, Smad3 phosphorylation and Kelch-like ECH-associated protein-1 (Keap1), and increased Nrf2, HO-1, cytoglobin, and PPARγ. In conclusion, DADS protects the kidney against Cd toxicity by attenuating OS, inflammation, and TGF-β1/Smad3 signaling, and enhancement of Nrf2/HO-1 signaling, antioxidants, and PPARγ.
•Cadmium induces oxidative stress, inflammation and fibrosis in rat kidney.•Diallyl disulfide prevents cadmium-induced nephrotoxicity.•Diallyl disulfide mitigates cadmium-induced oxidative stress and inflammation.•Diallyl disulfide downregulates TGF-β1/Smad3 and upregulated Nrf2/HO-1 signaling.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>39353227</pmid><doi>10.1016/j.tice.2024.102576</doi></addata></record> |
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| subjects | Allyl Compounds - pharmacology Animals Antioxidants - metabolism Antioxidants - pharmacology Cadmium Cadmium - toxicity Disulfides - pharmacology Garlic Heavy metals Inflammation Inflammation - chemically induced Inflammation - metabolism Inflammation - pathology Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney Diseases - chemically induced Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Diseases - prevention & control Male Nephrotoxicity NF-E2-Related Factor 2 - metabolism Oxidative stress Oxidative Stress - drug effects PPAR gamma - metabolism Protective Agents - pharmacology Rats Rats, Wistar Signal Transduction - drug effects Smad3 Protein - metabolism Transforming Growth Factor beta1 - metabolism Up-Regulation - drug effects |
| title | Attenuation of inflammation, oxidative stress and TGF-β1/Smad3 signaling and upregulation of Nrf2/HO-1 signaling mediate the protective effect of diallyl disulfide against cadmium nephrotoxicity |
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