Table II.

In vivo colitis models with rosemary extracts and essential oil

Model	Experimental conditions	Significant findings	Citation
TNBS-induced colitis rats	Animal strain: Wistar rats Study agent(s): Hydroalcoholic RE (100-400 mg/kg); REO (100-400 mg/kg)Groups (6 rats each): Method: Colitis was induced by administration of 80 mg/kg TNBS. Treatments were given 6 hours after TNBS administration and daily for 5 consecutive days	All treatments except 100 mg/kg RE and REO significantly reduced colonic damage scores, ulcer area, ulcer index, and width/length ratio Intraperitoneal administration was superior in reducing crypt damage and total colitic index compared to oral gavage	[30]
TNBS-induced colitis rats	Animal strain: Wistar rats Study agent(s): REO (2 mmol/kg); thyme essential oil (2 mmol/kg); turmeric essential oil (2 mmol/kg); broccoli extract (2 mmol/kg) Method: Treatments were given for 14 consecutive days with DSS exposure beginning on day 7. Colitis was induced by 4% DSS exposure in drinking water	No significant colitis development was detected in any group REO significantly increased expression of phase II-associated enzymes GSTK1, P1, T2, and the ARE-associated anti-oxidant enzyme GPx2 REO decreased the mRNA level of IL-10	[35]
DSS-induced colitis mice	Animal strain: Balb/C mice Study agent(s): RE (50 and 100 mg/kg) Method: Mice were fed RE in a 2% gum acacia matrix for 5 days before DSS exposure. Then, mice were fed RE for 5 additional days with DSS exposure (4%)	Both RE treatment groups reduced histological damage compared to DSS Treatment of RE decreased the MPO activity and levels of TNF-α and IL-6 RE reduced the nuclear translocation of Nf-κB protein, colonic levels of COX-2 and iNOS, and Nf-κB-DNA binding activity	[36]