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. 2018 May 8;33(3):261–269. doi: 10.1007/s12250-018-0031-4

Fig. 1.

Fig. 1

Recombinant Tat1–72 induces neurotoxicity in primary cultured neurons. (A) Recombinant Tat promoted HIV-1 LTR activation. Tat1–72 (3 μmol/L) was added to TZM-bl cells for 6 or 12 h, cells were lysed, and luciferase was detected using a GloMax system. Three replicates were sampled per treatment group in each of three independent experiments. Values are presented as mean ± SEM. *P < 0.05 versus 0 h group. (B) Tat decreased primary neuronal metabolic activity. Cultured neurons were treated with 1 mmol/L H2O2 or various concentrations of Tat1–72 (1, 2, 3, 4, or 5 μmol/L) for 24 h. H2O (5 μL) used as a control. Then, cell metabolic activity was detected using a CCK-8 kit. Five replicates were sampled per treatment group in each of three independent experiments. Values are presented as mean ± SEM. n = 3, *P < 0.05 versus control group. (C) Cultured neurons were treated with 5 μmol/L Tat1–72 or 5 μmol/L heat-inactivated Tat1–72 for 24 h. H2O (5 μL) used as a control. Then, cell metabolic activity was detected using a CCK-8 kit. Five replicates were sampled per treatment group in each of three independent experiments. Values are presented as mean ± SEM. n = 3, *P < 0.05 versus the control group.