Vitamin C Inhibits Lipopolysaccharide-Induced Hyperinflammatory State of Chronic Myeloid Leukemia Cells through Purinergic Signaling and Autophagy
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Tipo de produção
article
Data de publicação
2024
Título da Revista
ISSN da Revista
Título do Volume
Editora
MDPI
Autores
PIRES, Daniela A.
BRANDAO-RANGEL, Maysa A. R.
SILVA-REIS, Anamei
OLIMPIO, Fabiana R. S.
AIMBIRE, Flavio
OLIVEIRA, Carlos R.
MATEUS-SILVA, Jose R.
ZAMARIOLI, Lucas S.
BACHI, Andre L. L.
BELLA, Yanesko F.
Citação
NUTRIENTS, v.16, n.3, article ID 383, 14p, 2024
Resumo
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 mu g/mL and 10 mu g/mL) were employed, along with the lysosome inhibitor chloroquine (CQ; 100 mu M), administered 2 h prior to LPS stimulation (10 ng/mL) for a duration of 22 h in K-562 cells (3 x 10(5) cells/mL/well). Results: Both doses of vitamin C reduced the release of interleukin-6 (IL-6) (5 mu g/mL, p < 0.01 and 10 <mu>g/mL, p < 0.01) and tumor necrosis factor (TNF) (5 <mu>g/mL, p < 0.01 and 10 <mu>g/mL, p < 0.01) induced by LPS. Furthermore, in LPS + CQ-stimulated cells, vitamin C at a concentration of 10 <mu>g/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 <mu>g/mL, p < 0.01 and 10 <mu>g/mL, p < 0.01), while only the 10 <mu>g/mL dose of vitamin C induced the release of Klotho (10 mu g/mL, p < 0.01). In addition, both doses of vitamin C reduced the accumulation of ATP (5 <mu>g/mL, p < 0.01 and 10 <mu>g/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.
Palavras-chave
ascorbic acid, vitamin C, purinergic signaling, leukemia, autophagy, inflammation
Referências
- Agathocleous M, 2017, NATURE, V549, P476, DOI 10.1038/nature23876
- Alberca-Custódio RW, 2016, FRONT IMMUNOL, V7, DOI 10.3389/fimmu.2016.00237
- Aldapt MB, 2023, ONCOLOGY-BASEL, DOI 10.1159/000534266
- Almeida-Oliveira A R, 2019, Exerc Immunol Rev, V25, P50
- ALONSO S, 1986, J MOL EVOL, V23, P11, DOI 10.1007/BF02100994
- Aneja RK, 2011, MINERVA ANESTESIOL, V77, P986
- Balkwill F, 2009, NAT REV CANCER, V9, P361, DOI 10.1038/nrc2628
- Barbosa CMV, 2006, EUR J PHARMACOL, V542, P37, DOI 10.1016/j.ejphar.2006.06.004
- Bella YF, 2023, BIOMED PHARMACOTHER, V159, DOI 10.1016/j.biopha.2023.114263
- Bellodi C, 2009, J CLIN INVEST, V119, P1109, DOI 10.1172/JCI35660
- Bestach Y, 2019, LEUKEMIA RES, V86, DOI 10.1016/j.leukres.2019.106221
- Cimmino L, 2017, CELL, V170, P1079, DOI 10.1016/j.cell.2017.07.032
- Cojbasic I, 2023, MEDICINA-LITHUANIA, V59, DOI 10.3390/medicina59091564
- Couper KN, 2008, J IMMUNOL, V180, P5771, DOI 10.4049/jimmunol.180.9.5771
- Crowley LC, 2011, AM J HEMATOL, V86, P38, DOI 10.1002/ajh.21914
- Donadieu J, 2005, HAEMATOLOGICA, V90, P45
- Drill M, 2021, PURINERG SIGNAL, V17, P215, DOI 10.1007/s11302-021-09776-9
- Drullion C, 2012, CELL DEATH DIS, V3, DOI 10.1038/cddis.2012.111
- Ferrari D, 2000, FEBS LETT, V486, P217, DOI 10.1016/S0014-5793(00)02306-1
- Fitch BA, 2022, BLOOD ADV, V6, P854, DOI 10.1182/bloodadvances.2021005522
- Foster MN, 2018, ANTIOXIDANTS-BASEL, V7, DOI 10.3390/antiox7070092
- Garcia M, 2019, EUR J IMMUNOL, V49, P928, DOI 10.1002/eji.201847657
- Gillberg L, 2018, SEMIN CANCER BIOL, V51, P59, DOI 10.1016/j.semcancer.2017.11.001
- Silva LMG, 2016, PLOS ONE, V11, DOI 10.1371/journal.pone.0152890
- Holbrook Jonathan, 2019, F1000Res, V8, DOI 10.12688/f1000research.17023.1
- Huang XL, 2012, CANCER-AM CANCER SOC, V118, P3123, DOI 10.1002/cncr.26679
- Idzko M, 2014, NATURE, V509, P310, DOI 10.1038/nature13085
- Iwase S, 2019, AM J EMERG MED, V37, P260, DOI 10.1016/j.ajem.2018.05.040
- Razaul Karim M, 2017, BIOCHIMIE, V142, P51, DOI 10.1016/j.biochi.2017.08.004
- Larrouyet-Sarto ML, 2020, PURINERG SIGNAL, V16, P561, DOI 10.1007/s11302-020-09746-7
- Li Meng-Qi, 2015, Zhongguo Shi Yan Xue Ye Xue Za Zhi, V23, P583, DOI 10.7534/j.issn.1009-2137.2015.02.056
- Liu X, 2017, LEUKEMIA, V31, P2376, DOI 10.1038/leu.2017.108
- Liu YB, 2023, DIAB MET SYND CLIN R, V17, DOI 10.1016/j.dsx.2023.102854
- Mackenzie B, 2016, MED SCI SPORT EXER, V48, P1459, DOI 10.1249/MSS.0000000000000927
- Franco DM, 2019, COCHRANE DB SYST REV, DOI 10.1002/14651858.CD011811.pub2
- Pavlovsky C, 2023, J HEMATOL ONCOL, V16, DOI 10.1186/s13045-023-01440-6
- Portugal CC, 2021, FREE RADICAL BIO MED, V163, P43, DOI 10.1016/j.freeradbiomed.2020.11.039
- Prud'homme GJ, 2022, FRONT AGING-LAUSANNE, V3, DOI 10.3389/fragi.2022.931331
- Rinaldi I, 2023, J BLOOD MED, V14, P261, DOI [10.2147/JBM.S382090, 10.2147/JBM.S382090Journalof]
- Rothe K, 2019, INT J MOL SCI, V20, DOI 10.3390/ijms20030461
- Sachdeva A, 2020, CANCERS, V12, DOI 10.3390/cancers12061665
- Sáez PJ, 2017, SCI SIGNAL, V10, DOI 10.1126/scisignal.aah7107
- Sanchez-Correa B, 2013, CYTOKINE, V61, P885, DOI 10.1016/j.cyto.2012.12.023
- Schmid S, 2015, LUNG CANCER, V90, P516, DOI 10.1016/j.lungcan.2015.10.005
- Sharifzadeh S., 2023, Cardiovasc. Hematol. Agents Med. Chem, V21, P67, DOI [10.2174/1871525720666220819123639, DOI 10.2174/1871525720666220819123639]
- Shen N, 2019, ONCOTARGETS THER, V12, P2355, DOI 10.2147/OTT.S197535
- Shieh CH, 2014, GLIA, V62, P592, DOI 10.1002/glia.22628
- Singh P, 2021, MED ONCOL, V38, DOI 10.1007/s12032-021-01462-5
- Sun LR, 2022, DISCOV MED, V33, P93
- Tarumoto T, 2004, EXP HEMATOL, V32, P375, DOI 10.1016/j.exphem.2004.01.007
- Thompson DK, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0030659
- Wang L, 2020, CANCER CELL INT, V20, DOI 10.1186/s12935-020-1152-z
- Wang XS, 2014, CLIN CANCER RES, V20, P1366, DOI 10.1158/1078-0432.CCR-13-2442
- Willig JB, 2020, PURINERG SIGNAL, V16, P29, DOI 10.1007/s11302-019-09686-x
- Yan YL, 2017, MOL MED REP, V15, P1777, DOI 10.3892/mmr.2017.6172
- Yao X, 2014, PHARMACOL THERAPEUT, V141, P125, DOI 10.1016/j.pharmthera.2013.09.004
- Yu Y, 2012, LEUKEMIA, V26, P1752, DOI 10.1038/leu.2012.65
- Zhang LH, 2022, FRONT CELL INFECT MI, V12, DOI 10.3389/fcimb.2022.860526
- Zou D, 2018, BMC NEPHROL, V19, DOI 10.1186/s12882-018-1094-z