Table 3.

Summary of studies that evaluated the capacity of CGAs to modulate inflammatory stress in cell-based and animal-based models.

Models	End-Point Measure	CGA Isomer	Concentration/Exposure Time	Results Compared to the Control without CGA Treatment	References
Cell Models
Caco-2 + TNF-α and H2O2	IL-8	5-CQA	0.5–2 mM	↓ IL-8	[86]
Caco-2 + cocktail of inflammatory mediators	IL-6, IL-8	Mixture of all CGAs	Unknown composition of CGAs for 1 h	↓ IL-6, ↓ IL-8	[30]
RAW 264.7 + LPS	NO, IL-1β, TNF-α, cyclooxygenase-2, NF-κB, IL-6	5-CQA	2–20 μM for 24 h	↓ NO, ↓ IL-1β, ↓ TNF-α, ↓ IL-6, ↓ cyclooxygenase-2, ↓ NFκB	[87]
RAW 264.7 + LPS	Cyclooxygenase, Prostaglandin E2, NF-κB	5-CQA	12.5–37.4 μg/mL for 2 h	↓ Cyclooxygenase, ↓ Prostaglandin E2, ↓ NF-κB	[89]
Animal Models
Trinitrobenzenesulfonic acid induced colitis mice model	Myeloperoxidase, H2O2, NF-κB	5-CQA	Orally administration at 20 mg/kg body weight, twice a day for 6 days	↓ Myeloperoxidase, ↓ H2O2, ↓ NF-κB	[48]
Dextran sulfate sodium induced colitis mice model	IL-1β, TNF-α, macrophage inflammatory protein 2	5-CQA	Orally administration at 1 mM for 15 days	↓ IL-1β, did not significantly change the levels of TNF-α and macrophage inflammatory protein 2	[86]
Trinitrobenzenesulfonic acid induced colitis mice model	Myeloperoxidase, H2O2, NF-κB	5-CQA	Orally administration at 20 mg/kg body weight twice a day	↓ Myeloperoxidase, ↓ H2O2, ↓ NF-κB	[90]
Rheumatoid Arthritis rat model	IL-1β, TNF-α, T cells count, Th1 cytokines, Th2 cytokines	5-CQA	Orally administration at 40 mg/kg body weight	↓ IL-1β, ↓ TNF-α, ↓ T cells count, ↓ Th1 cytokines, ↑ Th2 cytokines	[91]
Wounds in diabetic rat	Wound healing speed, NO, MDA, GSH	5-CQA	Intraperitoneal injection at 50 mg/kg/day for 15 days	↑ Wound healing speed, ↑ GSH, ↓ NO, ↓ MDA	[92]
Liver injury rat model	MDA, GSH, TNF-α, NO, cyclooxygenase-2 protein increase	5-CQA	Orally administration at 2.5–10 mg/kg body weight, twice a day	↓ MDA, ↑ GSH, ↓ TNF-α, ↓ NO, ↓ cyclooxygenase-2 protein increase	[93]