Table 4.
Summary of anti-inflammatory activities of ginsenosides
| Ginsenosides | Activities | Models | Mode of action | Ref. |
|---|---|---|---|---|
| G-Rb1 | Anti-inflammation | LPS-treated RAW264.7 cells | Inhibiting TNF-α production | [30], [31] |
| LPS-treated murine peritoneal macrophages | Blocking activation of IRAL-1, IKK-β, NF-κB, and MAPKs | [32] | ||
| TNBS-induced colitis mice | Inhibiting IRAK-activated inflammatory response | [32] | ||
| Anti-osteoporosis | RANKL-treated osteoblasts differentiated from RAW264.7 cells | Blocking expression of c-Fos and NFATc1 by regulating RANKL-induced JNK, p38 MAPK, and NF-κΒ | [42] | |
| Compound K | Anti-inflammation | LPS-treated murine peritoneal macrophages | Blocking expression of proinflammatory cytokines by downregulating activities of IRAK-1, MAPKs, IKK-β, and NF-κB | [32] |
| LPS-treated RAW264.7 cells | Inhibiting expression of iNOS and COX-2 by suppressing NF-κB | [45] | ||
| Zymosan-treated RAW264.7 cells and BMDMs | Reducing proinflammatory cytokines, MAPKs, and ROS | [43] | ||
| TPA-induced ear edema mice | Inhibiting NF-κB and COX-2 | [46] | ||
| TNBS-induced colitis mice | Inhibiting NF-κB | [32] | ||
| DSS-induced colitis mice | Inhibiting NF-κB | [47] | ||
| Endotoxin-induced lethal shock mice | Decreasing expression of proinflammatory cytokines | [43], [48] | ||
| Anti-inflammation and neuroprotective effect | LPS-treated microglial cells | Suppressing ROS generation, MAPKs, NF-κB, and AP-1 | [44] | |
| G-Rb2 | Anti-inflammation | LPS-treated RAW264.7 and U937 cells | Inhibiting TNF-α production | [31] |
| Neuroprotective effect | LPS-treated N9 microglial cells | Suppressing TNF-α production via NF-κB inhibition | [49] | |
| G-Rd | Anti-inflammation | LPS-treated RAW264.7 cells | Reducing production of NO and PGE2, and NF-κB activity. | [51] |
| Neuroprotective effect | LPS-treated N9 cells | Suppressing TNF-α and NF-κB | [49] | |
| Transient focal cerebral ischemia rats | Inhibiting expression of iNOS and COX-2 | [50] | ||
| G-Re | Anti-inflammation | LPS-treated peritoneal macrophages | Blocking IKK-β phosphorylation, NF-κB activation, and production of proinflammatory cytokines | [52] |
| TNBS-induced colitis mice | Inhibiting NF-κB, IL-1β, and TNF-α | [52] | ||
| Anti-neuroinflammation | LPS-treated BV2-microglial cells | Suppressing iNOS, COX-2, and p38 MAPK | [55] | |
| G-Rg1 | Neuroprotective effect | LPS-treated BV-2 microglial cells | Suppressing iNOS, COX-2, TNF-α, IL-1β, and NF-κB via PLC-γ1 | [57] |
| LPS-injected rats | Inhibiting production of TNF-α, IL-1β, and NO via glucocorticoid receptor signaling | [58] | ||
| LPS-injected mice | Inhibiting expression of TNF-α, iNOS, and Iba-1 by blocking NF-κB and MAPKs | [56] | ||
| Anti-inflammation | LPS-treated RAW264.7 cells | (1) Suppressing IL-6 expression by inhibiting NF-κB (2) Increasing TNF-α expression by activation of Akt/mTOR |
[59] | |
| Alcohol-induced hepatitis mice | Inhibiting NF-κB | [60] | ||
| TNBS-induced colitis mice | Inhibiting NF-κB | [61] | ||
| Anti-ischemia reperfusion (IR) injury | Liver IR injury mice | Inhibiting NF-κB and ROS/NO/HIF | [62], [63] | |
| Cerebral IR injury rats | Activating PPAR-γ/HO-1 | [64] | ||
| Cerebral IR injury rats | Suppressing PAR-1 expression | [65] | ||
| Cerebral IR injury rats | Modulating p38 MAPK | [66] | ||
| G-Rg3 | Neuroprotective effect | Abeta42-treated BV-2 microglial cells | Inhibiting TNF-α expression and NF-κB activation | [67] |
| LPS-injected rats | Improving learning and memory impairment by inhibiting expression of proinflammatory mediators | [68] | ||
| Anti-inflammation | LPS-treated peritoneal macrophages and BMDMs | Suppressing S-nitrosylation of NLRP3 inflammasome by reducing NO generation and iNOS expression | [69] | |
| LPS-injected mice | Reducing susceptibility to lethal endotoxin shock by regulating NO generation | [69] | ||
| G-Rg5 | Anti-lung inflammation | LPS-treated alveolar macrophages | Decreasing expression of IL-1β, TNF-α, COX-2, and iNOS by inhibiting NF-κB pathway | [70] |
| TNF-α-treated HepG2 cells | Inhibiting NF-κB, COX-2, and iNOS | [71] | ||
| LPS-injected mice | Inhibiting TNF-α, IL-1β, iNOS, COX-2, and NF-κB | [70] | ||
| Anti-neuro inflammation | STZ-induced memory impaired rats | (1) Improving cognitive deficits by downregulating AChE activity and up-regulating ChAT activity (2) Increasing expression of BDNF and IGF-1 (3) Decreasing Aβ deposition (4) Suppressing COX-2 and iNOS |
[72] | |
| Scopolamine-induced memory impaired mice | Improving memory deficits by suppressing AChE activity and increasing BDNF expression and CREB phosphorylation | [73] | ||
| Anti-skin inflammation | TNF-α/IFN-γ-treated keratinocytes | Inhibiting expression of TARC/CCL17 via NF-κB/p38 MAPK/STAT signaling pathways | [74] | |
| LPS-treated RAW264.7 cells | Reducing generation of NO and ROS | [74] | ||
| G-Rh1 | Anti-neuro-inflammation | IFN-γ-treated BV2 microglial cells | Inhibiting iNOS expression by suppressing JAK/STAT, ERK, and NF-κB | [76] |
| Anti-skin inflammation | Oxazolone-induced atopic dermatitis-like mice | Suppressing production of IgE and IL-6, infiltration of inflammatory cells and granulation of mast cells | [77] | |
| G-Rh2 | Anti-neuroinflammation | LPS-/IFN-γ-treated BV-2 microglial cells | Reducing expression of iNOS, COX-2, TNF-α, and IL-1β by suppressing PKA/AP-1 | [78] |
| TNF-α-treated human astroglial cells | Inhibiting ICAM-1 expression by suppressing NF-κB and JNK/AP-1 | [79] | ||
| Anti-airway inflammation | OVA-induced asthma mice | Inhibiting peribronchiolar inflammation by suppressing NF-κB and p38 MAPK | [80] | |
| G-Rh2-B1/G-Rh2-B2 | Anti-inflammation | LPS-treated RAW264.7 cells | Reducing expression of TNF-α, IL-6, and IL-1β, and activities of p38 MAPK, JNK, and NF-κB | [81], [82] |
| G-Rp1 | Anti-inflammation | LPS-treated RAW264.7 cells | Reducing expression of IL-1β, COX-2, and iNOS by suppressing NF-symbolic kappaB | [83], [84] |
Aβ, amyloid beta; AChE, acetylcholinesterase; AP-1, activator protein-1; BDNF, brain derived neurotrophic factor; ChAT, choline acetyltransferase; COX-2, cyclooxygenase-2; DSS, dextran sulfate sodium; G-RB1, ginsenoside-Rb1; G-RB2, ginsenoside-Rb2; G-Rd, ginsenoside-Rd; G-Re, ginsenoside-Re; G-Rg1, ginsenoside-Rg1; G-Rg3, ginsenoside-Rg3; G-Rg5, ginsenoside-Rg5; G-Rh1, ginsenoside-Rh1; G-Rh2, ginsenoside-Rh2; G-Rp1, ginsenoside-Rp1; HIF, hypoxia-inducible factor; HO-1, heme oxygenase-1; ICAM-1, intercellular adhesion molecule 1; IFN, interferon; IKK, inhibitor of κB kinase; IL-6, interleukin-6; IL-1β, interleukin-1β; iNOS, inducible nitric oxide synthase; JNK, c-Jun N-terminal kinases; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-kappa B; NO, nitric oxide; OVA, ovalbumin; PKA, protein kinase A; TNBS, 2,4,6-trinitrobenzene sulfuric acid; TNF-α, tumor necrosis factor-alpha; TPA, 12-O-tetradecanoylphorbol-13-acetate.