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© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Background: Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the overproduction of white blood cells, leading to symptoms such as fatigue, infections, and other complications. CML patients must take measures to prevent infections to mitigate the exacerbation of cancer cell proliferation and comorbidities. Methods: This study investigated whether vitamin C can suppress the hyperinflammatory activation of K-562 cells induced by lipopolysaccharide (LPS) and whether purinergic signaling (ATP and P2X7 receptor) and autophagy play a role in it. Two different doses of vitamin C (5 µg/mL and 10 µg/mL) were employed, along with the lysosome inhibitor chloroquine (CQ; 100 µM), administered 2 h prior to LPS stimulation (10 ng/mL) for a duration of 22 h in K-562 cells (3 × 105 cells/mL/well). Results: Both doses of vitamin C reduced the release of interleukin-6 (IL-6) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) and tumor necrosis factor (TNF) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) induced by LPS. Furthermore, in LPS + CQ-stimulated cells, vitamin C at a concentration of 10 µg/mL inhibited the expression of LC3-II (p < 0.05). Conversely, both doses of vitamin C led to the release of the anti-inflammatory cytokine interleukin-10 (IL-10) (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01), while only the 10 µg/mL dose of vitamin C induced the release of Klotho (10 µg/mL, p < 0.01). In addition, both doses of vitamin C reduced the accumulation of ATP (5 µg/mL, p < 0.01 and 10 µg/mL, p < 0.01) and decreased the expression of the P2X7 receptor at the mRNA level. Conclusions: Vitamin C inhibits the hyperinflammatory state induced by LPS in K-562 cells, primarily by inhibiting the ATP accumulation, P2X7 receptor expression, and autophagy signaling.

Details

Title
Vitamin C Inhibits Lipopolysaccharide-Induced Hyperinflammatory State of Chronic Myeloid Leukemia Cells through Purinergic Signaling and Autophagy
Author
Pires, Daniela A 1 ; Brandão-Rangel, Maysa A R 2   VIAFID ORCID Logo  ; Silva-Reis, Anamei 2 ; Olímpio, Fabiana R S 3 ; Aimbire, Flavio 3   VIAFID ORCID Logo  ; Oliveira, Carlos R 4   VIAFID ORCID Logo  ; Mateus-Silva, José R 4   VIAFID ORCID Logo  ; Zamarioli, Lucas S 5   VIAFID ORCID Logo  ; Bachi, André L L 6   VIAFID ORCID Logo  ; Bella, Yanesko F 2 ; Santos, Juliana M B 2   VIAFID ORCID Logo  ; Bincoletto, Claudia 5   VIAFID ORCID Logo  ; LanchaJr, Antonio Herbert 7 ; Vieira, Rodolfo P 8   VIAFID ORCID Logo 

 Post-Graduation Program in Bioengineering, Universidade Brasil, Rua Carolina Fonseca 235, São Paulo 08230-030, SP, Brazil; [email protected] 
 Postgraduate Program in Science of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos 11060-001, SP, Brazil; [email protected] (M.A.R.B.-R.); [email protected] (A.S.-R.); [email protected] (Y.F.B.); [email protected] (J.M.B.S.) 
 Department of Medicine, Postgraduate Program in Translational Medicine, Federal University of São Paulo (UNIFESP), Rua Pedro de Toledo 720, Vila Clementino, São Paulo 04039-002, SP, Brazil; [email protected] (F.R.S.O.); [email protected] (F.A.) 
 Gap Biotech Laboratory of Biotechnology and Bioinformatics, Rua Comendador Remo Cesaroni 223, São José dos Campos 12243-020, SP, Brazil; [email protected] (C.R.O.); [email protected] (J.R.M.-S.) 
 Department of Pharmacology, Federal University of São Paulo (UNIFESP), Rua Três de Maio 100, São Paulo 04044-020, SP, Brazil; [email protected] (L.S.Z.); [email protected] (C.B.) 
 Postgraduate Program in Health Science, Santo Amaro University, Rua Prof. Enéas de Siqueira Neto 340, São Paulo 04829-300, SP, Brazil; [email protected] 
 Experimental Surgery (LIM 26), Laboratory of Clinical Investigation, School of Medicine, University of Sao Paulo, Avenida Doutor Arnaldo 455, São Paulo 05508-030, SP, Brazil; [email protected] 
 Post-Graduation Program in Bioengineering, Universidade Brasil, Rua Carolina Fonseca 235, São Paulo 08230-030, SP, Brazil; [email protected]; Postgraduate Program in Science of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos 11060-001, SP, Brazil; [email protected] (M.A.R.B.-R.); [email protected] (A.S.-R.); [email protected] (Y.F.B.); [email protected] (J.M.B.S.); Gap Biotech Laboratory of Biotechnology and Bioinformatics, Rua Comendador Remo Cesaroni 223, São José dos Campos 12243-020, SP, Brazil; [email protected] (C.R.O.); [email protected] (J.R.M.-S.); Postgraduate Program in Human Movement and Rehabilitation and in Pharmaceutical Sciences, Evangelical University of Goiás (Unievangélica), Avenida Universitária Km 3,5, Anápolis 75083-515, GO, Brazil 
First page
383
Publication year
2024
Publication date
2024
Publisher
MDPI AG
e-ISSN
20726643
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2923936317
Copyright
© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.