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. 2023 Oct 5;6(12):e202302148. doi: 10.26508/lsa.202302148

Figure 8. SP600125 reverses HIV-1–induced M1 polarization by inhibiting JNK activation.

Figure 8.

Monocyte-derived macrophages (MDMs) were pretreated with or without SP600125 (50 μM) for 2 h, followed by infection of HIV-1 for 48 h. (A) Expressions of JNK and COX-2 were measured by Western blot. Total JNK was used as the normalization control of phosphorylated JNK, and β-actin was used as the normalization control of COX-2. (Statistical analysis was performed using a t test, *P < 0.05, **P < 0.01, and ***P < 0.001.) (B) Western blot analysis of hypoxia-inducible factor 1α, HK1, HK2, and LDHA in MDMs. β-Actin was used as the normalization control. SP600125, meloxicam, LW6, and YC-1 were administered as mentioned above. (Statistical analysis was performed using a t test, *P < 0.05 and **P < 0.01 as compared to Control; #P < 0.05, ##P < 0.01, and ###P < 0.001 as compared to HIV-1.) (C) Lactate concentration in the culture supernatant of MDMs was detected using colorimetry. (Statistical analysis was performed using a t test, *P < 0.05 and ***P < 0.001.) (D, E) MDMs were collected, and the expression of TNF-α, IL-1β, and IL-6 was measured by RT–qPCR (D) and ELISA (E). (Statistical analysis was performed using a t test, *P < 0.05, **P < 0.01, and ***P < 0.001).