The ameliorative effect of (-)-epigallocatechin-3-gallate (EGCG) on inflammatory bowel disease (IBD) induced by ethanol 2,4,6-trinitrobenzene sulfonic acid (TNBS) was studied in 7-week-old male rats. Intestinal lesions were measured as an increase in myeloperoxidase (MPO) activity in mucosa. The supplementation of EGCG significantly inhibited MPO activity and histamine levels in the distal colon mucosa. The EGCG inhibited macrophage chemotaxis toward N-formyl-L-methionyl-L-leucyl-L-phenylalanine in a concentration-dependent manner. These observations confirmed that EGCG can ameliorate acute experimental colitis by the suppression of mast cells and macrophage activities.

Oxidative stress is considered as a mechanism of hepatocellular injury in non-alcoholic steatohepatitis (NASH). Pycnogenol (PYC) is the natural plant extract from the bark of Pinus pinaster Aiton. and has potent antioxidant activities. We studied the protective effect of PYC on excessive fat accumulation in the liver fed a methionine-choline deficient (MCD) high-fat diet for 6 weeks. Pycnogenol (10 mg/kg body weight) was orally administered for 5 weeks. At the end of the experiment, blood and liver samples were collected and assessed for effects of PYC by histopathological and biochemical analyses. Histopathological analyses of liver tissues stained with Azan-Mallory showed hepatic macrovesicular steatosis and fibrosis in MCD-fed rats. Supplementation of PYC prevented this effect. Pycnogenol treatment significantly decreased the liver triglyceride and serum alanine amino transferase levels. Our results indicated that orally administered PYC may serve to prevent NASH-induced liver damage.

The influence of catechins in green tea on lipolysis in fully differentiated 3T3-L1 cells was studied and glycerol release into the buffer, cytosol and residual triglyceride were measured. The addition of (-)-epigallocatechin-3-gallate (EGCG) stimulated glycerol release into the cytosol significantly after incubation for 4 h, but had no effect on that into the buffer. However, (+)-catechins did not produce a significant increase in lipolysis. These data suggested that EGCG has strong lipolytic activity.

Pycnogenol was administered for 10 days by gavage to Sprague-Dawley rats fed an elemental diet, then inflammatory bowel disease (IBD) was induced by intrarectal administration of ethanol 2,4,6-trinitrobenzene sulfonic acid (TNBS). Twelve hours after TNBS treatment, the rats were killed, the colon was assessed by a macroscopic damage score and mucosa homogenate was assayed for myeloperoxidase (MPO) activity. The supplementation of pycnogenol significantly inhibited the macroscopic damage score and MPO activity in a dose-dependent manner. These results suggested that pycnogenol ameliorates TNBS-induced inflammation by radical scavenging activity, and may have beneficial effects as a supplement in enteral nutrition for IBD.

EHCG may have therapeutic benefit as a supplement in enteral nutrition for patients with inflammatory bowel diseases.