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. 2021 May 7;12:675287. doi: 10.3389/fphar.2021.675287

FIGURE 4.

FIGURE 4

Potential curcumin in cell damage caused by SARS-CoV-2 in the lung and heart. Curcumin promotes differentiation from naïve CD4+T-cell to Tregs through the modulation of IL-10 (1). The cytoprotective role of curcumin decreases the death of type II alveolar cells (ATII) with a consequent decrease in the release of DAMPs (2). Curcumin also mediates macrophages' polarization, decreasing the population of inflammatory macrophages M1 to macrophages M2 that participate in the resolving and reparative process (3). The presence of Th17 cells promotes the activation of ATII cells through IL-17. In turn, activated ATII cells release a chemoattractant for neutrophils that causes neutrophil aggregation. Curcumin decreases IL-17 levels with a consequent decrease in neutrophil aggregates. The anticoagulant and antithrombotic effects of curcumin can have protective effects on the heart, decreasing the heart attack risk (5). The anti-inflammatory action of curcumin can prevent damage to cardiomyocytes caused by an excess of inflammatory mediators, known as a cytokine storm (6). Its affinity for protein S and ACE2 can prevent the direct infection of cardiomyocytes by SARS-CoV-2 (7). Abbreviations: ATII, alveolar type II cells; Tregs, regulatory T cells; Th17, T helper 17 cells; CXCL-1, chemokine ligand 1; NET, neutrophil extracellular traps.