Table 3.
Summary of the therapeutic effects of ginsenoside against sepsis.
|
Ginsenoside |
Dosage and administration route | Effects | Experimental models | Ref. |
|---|---|---|---|---|
| Rb1 | 5 mg/kg/h 60 min, i.v. | Decrease of NF-κB activity and proinflammatory molecules | LPS-induced ALI in male Wistar rats | [44] |
| 20 mg/kg, i.g. | Inhibit IL-1β, IL-6 and TNF-α production | (S. aureus)-induced ALI in Kunming male mice | [47] | |
| 40 mg/kg, i.g. | Downregulate the expression of TLR4 mRNA and inhibited the production of TNF-α | septic shock in SD rats | [48] | |
| Rb2 | / | Inhibit TNF-α and IL-6 production | LPS-stimulated RAW 264.7 cells | [45] |
| Re | 10, 20 mg/kg, i.g. | Inhibit the expression of proinflammatory cytokines TNF-α and IL-1β | LPS-induced inflammation in male ICR mice | [50] |
| 20 mg/kg, i.g. | Prevent NF-κB and MAPK activation | LPS-induced ALI in male ICR mice | [53] | |
| CK | 20, 30, 40 μM | suppressed phosphorylation of IκB-α and NF-κB, MAPK activation | LPS-treated RAW264.7 cells | [54] |
| 50 mg/kg, 3 d, i.g. | Reduced the levels of inflammatory cytokines TNF-α and IL-6 | Endotoxin-induced lethal shock in male C57BL/6 mice | [56] | |
| Rh1 | 10, 25, 50 μM | inhibited iNOS, COX-2 protein expression and the activation of NF-κB | LPS-treated RAW264.7 cells | [58] |
| 126 or 252 μg/mouse, i.v.) | Suppressed the production of TNF-α, IL-6, activation of NF-κB and ERK 1/2 by HMGB1 | CLP model in male C57BL/6 mice | [62] | |
| DEX (1 μM) with Rh1 (10 μM, 1 μM, 0.1 μM) | Inhibit the transcription of pro-inflammatory genes via suppression of the transcriptional activation induced by AP-1 and NFκB | RAW264.7 cells | [61] | |
| Rh2 | 10, 20, 30 mg/kg, i.g. | blocked iNOS, COX-2, the phosphorylation of IκB-α, ERK, JNK, p38, protein expression | LPS-induced ALI in male ICR mice | [63] |
| Rg1 | 15, 30, 60 mg/kg, i.g. | Inhibit the protein expression of TLR4 and its downstream genes including NF-κB and MAPKs | (LPS/D-GalN)-induced ALI in C57BL/6 mice | [68] |
| 20 μM | Revers the increased expression of TLR4, NF-κB, and NLRP3 | Neonatal rat cardiomyocytes | [70] | |
| 10 μM | Attenuate NF-κB cytoplasmic-to-nuclear translocation and downregulation of MAPK phosphorylation | RAW264.7 cells | [72] | |
| Rg5 | 5, 10 μM | Inhibited the phosphorylation of NF-κB | Male C57BL/6 mice alveolar macrophages | [73] |
| 10, 20, 40 μM | suppressing the production of TNF-α and IL-6 and the activation of NF-κB and ERK 1/2 | Primary human umbilical vein endothelial cells (HUVECs) | [74] | |
| Rg3 | 10 mg/kg, i.g | Inhibit IL-1β production via the S-nitrosylation of the NLRP3 inflammasome | LPS-induced endotoxic shock in male C57BL/6 mice | [76] |
| 10 mg/kg, 3 d, i.g. | reduced the level of IL-1βand TNF-α production | C57BL/6 J mice | [77] | |
| 10, 20 mg/kg, i.g. | Improve mitochondrial dysfunction | CLP-induced sepsis male C57BL/6 mice | [80] | |
| 10, 20, 30 mg/kg, i.g. | Decrease the levels of pro-inflammatory mediators and increasing the production of anti-inflammatory cytokines | LPS-induced ALI in male C57Bl/6 mice | [81] |