Figure 1 | Scientific Reports

Figure 1

From: The binding capability of plasma phospholipid transfer protein, but not HDL pool size, is critical to repress LPS induced inflammation

Figure 1

The role of PLTP on endotoxic shock status in mice.

(A) Before LPS injection, plasma PLTP activity of wild type mice (WT, N = 5), PLTP transgenic mice (PLTP-Tg, N = 5) and PLTP knockout mice (PLTP−/−, N = 5) were determined through the fluorescent phospholipids transferring from donor to acceptor particles (See method for detail).*P < 0.05 for PLTP-Tg VS. WT; #P < 0.05 for PLTP−/− VS. WT. (B) Pooled plasma (100 μL) from 4 or 5 mice of each genotype were fractionated by fast protein liquid chromatography (FPLC). Cholesterol level were determined and plotted as a function of FPLC fractions. The fractions containing lipoproteins are indicated. (C) Upper panel: plasma apoAI levels from PLTP−/−, WT, or PLTP-Tg were detected by western blot (WB). Lower panel: Densitometric quantitation of WB (n = 4), *P < 0.05 VS. WT. **P < 0.01 VS. WT. (D) HDL-C levels were assayed before and after LPS intraperitoneal injection. (WT, 6 mg/Kg, N = 10; PLTP-Tg, 6 mg/Kg, N = 10; PLTP−/−, 5 mg/Kg, N = 10.) (E) Compared with WT, PLTP-Tg showed a higher survival rate after LPS injection for 9 days, while PLTP−/− displayed nearly 10% survival individuals after LPS injection. Survival rates were analyzed by the Kaplan-Meier method and compared using the X2 test. *P < 0.05 for PLTP-Tg VS. WT; #P < 0.05 for PLTP−/− VS. WT.

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