Immunoregulatory activity |
Aeps |
Raw264.7cells |
Cells |
Induced the activation of macrophages via lncrnas/nf-κb networks |
50 μg/ml |
4 h |
Chen et al. (2019a)
|
AEPS |
RAW264.7cells |
Cells |
Induced macrophage activation through regulating mirnas expression |
50 μg/ml |
24 h |
Chen et al. (2019b)
|
AEPS |
Mice |
Supernatant and the elleted cells |
Induced the expression of large numbers of cytokines and chemokines |
50 μg |
3, 6 h |
Du et al. (2020)
|
AEPS |
RAW264.7 cells |
Cells |
Enhanced the pinocytic and phagocytic activity, promote the expression of accessory and costimulatory molecules |
0–200 μg/ml |
24 h |
Sun et al. (2015)
|
AEPS |
Icrmice |
Sera and splenocyte |
Increased both cellular and humoral immune responses and elicited a balanced Th1/Th2 response |
25,50, 100 μg |
2 weeks |
Sun et al. (2009)
|
Phenoplic extracts |
Splenocyte |
Cell |
Induced the proliferation and reduced IFN-γ production |
62.5–1,000 μg/ml |
48 h |
Kim et al. (2018)
|
Antitumor activity |
Eel, ees |
Huvecs |
Cells |
Decreased the Cell viability |
100 μg/ml |
24 h |
Wu et al. (2017)
|
EER |
SGC7901 cells, CNE2 cells and huvecs |
Cells |
Inhibited the cells’ growth |
100 μg/ml |
24 h |
Wu et al. (2017)
|
PE-EER, BA-EER, WE-EER |
Huvecs |
Cells |
Inhibited the cells’ growth |
100 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
CNE2 cells |
Cells |
Inhibited the cells’ growth |
100 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
SGC7901 cells, huvecs |
Cells |
Inhibited the cells’ growth in a time and dose-dependent manner |
0–100 μg/ml |
24, 48, 72 h |
Wu et al. (2017)
|
EA-EER |
SGC7901 cells |
Cells |
Decreased the Number of cells and ncreasing degree of apoptosis with some obvious apoptotic morphological alterations |
0, 50, 75 and 100 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
Huvecs |
Cells |
Induced apoptosis |
0, 40, 60, 80 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
Huvecs |
Cells |
Inhibit cell migration of huvecs in a dose-dependent manner |
0, 30, 40, 60 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
Chick CAM model |
Blood vessels |
Was capable of restraining angiogenesis in vivo
|
1.0 mg/ml |
72 h |
Wu et al. (2017)
|
AEPS and AEPA, AEPB, AEPC, AEPD |
Tumor-bearing mice |
Tumors |
Inhibited the growth of tumor transplanted |
2.5, 5.0, 10.0 mg/kg |
10 days |
Xu et al. (2009b)
|
AEPS and AEPA, AEPB, AEPC, AEPD |
S180-bearing mice |
S180 sarcoma |
Inhibited the growth of transplantable S180 sarcoma in mice and promoted splenocytes proliferation, natural killer cells activity, interleukin-2 production from splenocytes and serum tumor antigen-specific antibody levels in tumor-bearing |
10 mg/kg |
5 days |
Xu et al. (2009a)
|
Anti-angiogenic activity |
Ea-eer |
Sgc7901 cells |
Cells |
Downregulated mrna expression of bcl-2 and up-regulated mrna expression of bcl-2 and the protein expression of caspase-3in sgc7901 cells, in a dose-dependent manner |
0, 40, 60, 80 μg/ml |
24 h |
Wu et al. (2017)
|
EA-EER |
Huvecs |
Cells |
Reduced mrna expression of VEGF-A and VEGFR-2 in huvecs |
0, 40, 60, 80 μg/ml |
24 h |
Wu et al. (2017)
|
Neuroprotective activity |
Aqueous ethanol |
Pc-12 cells |
Cells |
Protected neuron-like pc-12 cells from aβ1-42 -induced neurotoxicity |
62.5, 250, and 1,000 μg/ml |
24 h |
Cho et al. (2021)
|
Aqueous ethanol |
ICR mice |
Mice |
Prevented cognitive impairment |
50, 200, and 1,000 mg/kg |
3 weeks |
Cho et al. (2021)
|
Aqueous ethanol |
ICR mice |
Brain tissue |
Ameliorated Aβ1-42 -induced spatial cognitive learning and memory deficits and protected the antioxidant defense systems in brain tissue |
50, 200, and 1,000 mg/kg |
3 weeks |
Cho et al. (2021)
|
Anti-inflammatory activity |
Phenolic extracts |
Macrophages |
Cells |
Inhibited the production of the pro-inflammatory cytokines |
62.5–1,000 μg/ml |
48 h |
Kim et al. (2018)
|