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. 2022 May 7;47(1):1–8. doi: 10.1016/j.jgr.2022.05.004

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]