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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Phytosomal curcumin causes natural killer cell-dependent repolarization of glioblastoma (GBM) tumor-associated microglia/macrophages and elimination of GBM and GBM stem cells

Fig. 4

Peripheral injection of the NK cell-neutralizing NK1.1 antibody partially reverses the CCP-mediated M2➔M1 repolarization, IL10 suppression, and IL12 induction in TAM. a The dispersed Iba1(+) cells in the CCP-treated GBM displayed an 80% decrease in integrated ARG1 fluorescence with respect to the Vehicle-treated (*p = 0.01, Vehicle versus CCP) and this decrease was only 60% in the CCP + NK1.1 samples (Δ p = 0.03, CCP versus CCP + NK1.1; **p = 0.02, Vehicle versus CCP + NK1.1) (a i-v). Compared to the iNOS IF values in the Vehicle-treated, the Iba1(+) cells in the other two groups displayed a 293% increase in the CCP-treated (*p = 0.004, CCP versus Vehicle) and an 89% increase in the CCP + NK1.1-treated (Δ p = 0.014 CCP + NK1.1 versus CCP; **p = 0.04, Vehicle versus CCP + NK1.1) (b i-v). The graphs represent mean ± S.D. for iNOS/ARG1 obtained from Vehicle (n = 4), CCP (n = 4), and CCP + NK1.1 (n = 3) mice. c-f The Iba1(+) cells displayed a 92% decrease IL10 IF in the CCP-treated (*p = 8.7 × 10− 6, CCP versus Vehicle) and only a 65% decrease in the CCP + NK1.1-treated samples (Δ p = 0.03, CCP + NK1.1 versus CCP; **p = 5.0 × 10− 3, Vehicle versus CCP + NK1.1) (c i - iv and e). The Iba1(+) cells displayed a 445% increase in IL12 IF in the CCP-treated mice (*p = 0.01, CCP versus Vehicle) and a 69% increase in the CCP + NK1.1 mice (Δ p = 0.01, CCP + NK1.1 versus CCP; **p = 0.04, Vehicle versus CCP + NK1.1) (d i-iv and f). The graphs represent mean ± S.D. obtained from Vehicle (n = 4), CCP (n = 4), and CCP + NK1.1 (n = 3) mice

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