ABSTRACT
Objective To observe the impact of modified Liangge powder (MLP) on platelet activation markers and the release of proinflammatory cytokine in mice by stimulation of lipopolysaccharide (LPS). Methods 112 male mice were randomly divided into control group, model group and MLP low, middle and high dose treatment groups. The sepsis model was reproduced by injection of LPS 10 mg/kg into a mouse tail vein. In the control group, normal saline 10 mg/kg was injected into the tail vein of mouse. The MLP low, middle, and high dose groups received 0.94, 1.89, 2.84 g/mL MLP 0.02 mL/g by gavage respectively for 3 days, while the control group and model group received equal amount of normal saline by gavage for 3 days. After modeling for 24 hours and 72 hours, 8 mice in each of the three different dose MLP groups and model group were killed and their blood was taken. In the control group, after modeling for 24 hours, 8 mice were killed and their blood was taken. Platelet (PLT) was counted by blood cell analyzer, plasma interleukin-10 (IL-10), high mobility group protein B1 (HMGB1) and platelet factor 4 (PF4) were detected by enzyme-linked immunosorbent assay (ELISA). In each group after modeling for 72 hours, another 8 mice were taken, and laser scanning confocal microscopy was used to measure the platelet cytosolic Ca2+ concentration. Results Compared with the control group, the level of PLT at 24 hours(×109/L: 347.70±115.10 vs. 1 013.10±136.60) was decreased, and the levels of IL-10 (μg/L: 356.86±34.72 vs. 39.50±23.45), HMGB1 (mg/L: 16.24±4.49 vs. 10.75±1.91), PF4 (μg/L: 5.43±0.61 vs. 1.33±0.40) and Ca2+ (nmoL/L: 8.60±0.52 vs. 1.05±0.33) were elevated in model group. Compared with the model group, the levels of PLT in the MLP high, middle and low dose groups were all significantly elevated; the increase in PLT in middle dose group after modeling for 72 hours was the most remarkable (×109/L:952.13±104.02 vs. 771.50±129.30, P < 0.05); the levels of IL-10, HMGB1, PF4, Ca2+ in MLP low, middle, high dose groups were significantly decreased. The most obvious degree of decrease in level of the following indexes were as follows:IL-10 in MLP high dose group at 72 hours after modeling (μg/L:110.17±29.12 vs. 441.50±30.72), HMGB1 in MLP high dose group after modeling for 24 hours (mg/L: 10.33±3.52 vs. 16.24±4.49), PF4 in MLP middle dose group after modeling for 24 hours (μg/L:2.08±0.92 vs. 5.43±0.61) and Ca2+ in MLP high dose group (nmoL/L:2.97±0.96 vs. 8.60±0.52, all P<0.05). Conclusion MLP may possibly down-regulate the inflammatory cytokines release induced by LPS to inhibit the activation of platelet Ca2+, in turn prevent the activation of platelet and improve thrombocytopenia caused by LPS.
