Pyrrolidine dithiocarbamate inhibits UVB-induced skin inflammation and oxidative stress in hairless mice and exhibits antioxidant activity in vitro

Ivan, Ana L.M.; Campanini, Marcela Zambrim; Martínez, Renata M.; Ferreira, Vitor S.; Steffen, Vinicius S.; Vicentini, Fabiana T. M. C.; Vilela, Fernanda Maria Pinto; Martins, Frederico Severino; Zarpelon, Ana C.; Cunha, Thiago M.; Fonseca, Maria José Vieira; Baracat, Marcela M.; Georgetti, Sandra R.; Verri, Waldiceu A.; Casagrande, Rúbia

doi:10.1016/j.jphotobiol.2014.05.010

Cited by 63 publications

(92 citation statements)

References 59 publications

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“…In fact, inhibiting NFkB activation with drugs such as PDTC (pyrrolidine dithiocarbamate) reduces cytokine production in varied models of inflammation (Ivan et al, 2014;Schreck et al, 1992). In agreement with the role of cytokines in pain, inhibiting NFkB activation also reduces pain (Possebon et al, 2014;Tegeder et al, 2004).…”

Section: Introductionmentioning

confidence: 82%

“…In addition to the inhibitory effect of PDTC over NFkB activation, it has been reported that PDTC presents antioxidant effect (Ivan et al, 2014). Evidence support that the antioxidant effect of PDTC explains its inhibitory action over NFkB (Schreck et al, 1992) as well as PDTC presents antioxidant effects without inhibiting NFkB activation (Nathens et al, 1997).…”

Section: Discussionmentioning

confidence: 97%

“…injection of carrageenan (300 mg/paw) with sample collection at 3 h was used as a positive control. Doses of treatment were based on previous studies of our group and standardization in our laboratory (Borghi et al, 2014a(Borghi et al, , 2014bCarvalho et al, 2015, Carvalho et al, 2011Ivan et al, 2014).…”

Section: Experimental Protocolsmentioning

confidence: 99%

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Jararhagin-induced mechanical hyperalgesia depends on TNF-α, IL-1β and NFκB in mice

Ferraz

Calixto-Campos

Manchope

et al. 2015

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Jararhagin is a hemorrhagic metalloprotease from Bothrops jararaca snake venom. The hyperalgesic mechanisms of jararhagin were investigated focusing on the role of proinflammatory cytokines (TNF-α and IL-1β) and the transcription factor NFκB. Intraplantar administration of jararhagin (1, 10, 100 and 1000 ng/paw) induced mechanical hyperalgesia, and increased TNF-α levels at 1, 3 and 5 h, and IL-1β levels at 0.5, 1 and 3 h after its injection in the paw tissue. Pre-treatment with morphine (2, 6, 12 μg/paw) inhibited jararhagin-induced mechanical hyperagesia. The systemic or local pre-treatment with etanercept (10 mg/kg and 100 μg/paw) and IL-1ra (30 mg/kg and 100 pg/paw) inhibited jararhagin-induced mechanical hyperalgesia. Co-administration of jararhagin (0.1 ng/paw) and TNF-α (0.1 pg/paw) or jararhagin (0.1 ng/paw) and IL-1β (1 pg/paw) enhanced the mechanical hyperalgesia. The systemic or local pre-treatment with PDTC (NFκB inhibitor; 100 mg/kg and 100 μg/paw) inhibited jararhagin-induced mechanical hyperalgesia as well as PDTC decreased the jararhagin-induced production of TNF-α and IL-1β. Thus, these data demonstrate the involvement of pro-inflammatory cytokines TNF-α and IL-1β and nuclear transcription factor NFκB in jararhagin-induced mechanical hyperalgesia indicating that targeting these mechanisms might contribute to reduce the pain induced by B. jararaca snake venom.

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Section: Introductionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 97%

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Jararhagin-induced mechanical hyperalgesia depends on TNF-α, IL-1β and NFκB in mice

Ferraz

Calixto-Campos

Manchope

et al. 2015

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“…PDTC has been used to suppress the activity of NF-kB in vivo and in vitro [54,55]. It has been previously reported that the dithiocarbamates stand for a class of antioxidants reported to be potent inhibitors of NF-κB.…”

Section: Discussionmentioning

confidence: 99%

Buthionine sulfoximine, an inhibitor of glutathione biosynthesis, induces expression of soluble epoxide hydrolase and markers of cellular hypertrophy in a rat cardiomyoblast cell line: Roles of the NF-κB and MAPK signaling pathways

Abdelhamid

El‐Kadi

2015

Free Radical Biology and Medicine

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“…Additionally, PDTC has effective anti-inflammatory and anti-tumor properties [14]. Previously, several studies have shown that PDTC can affect inflammation, such as by inhibiting ultraviolet B-induced skin inflammation and by preventing neuroinflammation and cognitive dysfunction after endotoxemia [15,16]. However, few studies have clarified the relationships among PDTC, TLR4, NF-κB and peri-implantitis.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Jiang²,

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The roles of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in peri-implantitis are unclear. Here, we used a canine model of peri-implantitis to explore the effects of inhibiting NF-κB with pyrrolidine dithiocarbamate (PDTC) on the inflammatory response in ligature-induced peri-implantitis. Methods: After successfully establishing the peri-implantitis model, beagles were randomly assigned to normal, model or PDTC groups. ELISA tests were used to determine the levels of interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). Immunohistochemistry was employed to assess the expression of NF-κB p65. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the mRNA levels of TLR4 and NF-κB p65, and western blot analysis was used to measure the protein levels of TLR4 in periodontal tissues from each group. Periodontal ligament fibroblasts (PDLFs) were cultured and subsequently classified into PDLF normal, PDLF model, PDLF LPS, PDLF PDTC, and PDLF LPS + PDTC groups. An immunofluorescence assay was used to measure the expression level of NF-κB p65. The CCK-8 assay and flow cytometry were performed to evaluate cell proliferation and apoptosis. Results: The in vitro results indicated that NF-κB p65 and TLR4 were upregulated in canine periodontal tissues, and PDTC could suppress the expression levels of NF-κB p65 and TLR4. Inflammation could increase TLR4 protein expression in canine periodontal tissue, and PDTC could inhibit the inflammation-induced increase in TLR4 protein expression. These results revealed that PDTC could reverse the LPS-induced increases in the levels of IL-1, IL-6, IL-8 and TNF-α. In vivo, the results demonstrated that PDTC inhibited the LPS-induced NF-κB p65 upregulation, and PDTC could reverse the inhibitory effect of the PDLF model + LPS on the proliferation of periodontal fibroblasts. The results also showed that in the PDLF model, LPS promoted PDLF apoptosis by inducing implant periodontitis in canines, but PDTC inhibited the PDLF apoptosis and relieved implant periodontitis in canines. Conclusion: Based on our results, we concluded that PDTC can inhibit the expression of NF-κB and alleviate the inflammatory response induced by LPS, thereby preventing periodontal inflammation and reducing the development of peri-implantitis.

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Pyrrolidine dithiocarbamate inhibits UVB-induced skin inflammation and oxidative stress in hairless mice and exhibits antioxidant activity in vitro

Cited by 63 publications

References 59 publications

Jararhagin-induced mechanical hyperalgesia depends on TNF-α, IL-1β and NFκB in mice

Jararhagin-induced mechanical hyperalgesia depends on TNF-α, IL-1β and NFκB in mice

Buthionine sulfoximine, an inhibitor of glutathione biosynthesis, induces expression of soluble epoxide hydrolase and markers of cellular hypertrophy in a rat cardiomyoblast cell line: Roles of the NF-κB and MAPK signaling pathways

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

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