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.

The improved effect of Pycnogenol on impaired spatial memory function was studied in orchidectomized rats. Endogenous testosterone levels were decreased by approximately one-half for 3 months after castration. In the radial arm maze, castration significantly impaired working and reference memory function without lowering motor function. Pycnogenol increased the NGF content in the hippocampus and cortex, and improved the spatial memory impairment. These observations confirmed that diagnostic accuracy can be improved by Pycnogenol in androgen-deficient rats.

We studied the influence of (+)- and (-)-catechin contained in green tea on insulin induced lipogenesis in 3T3-L1 cells. In 14 days of culture with insulin, the intracellular triglyceride concentration and the activities of glycerophosphate dehydrogenase, a marker of adipose conversion, increased. The addition of 0.02 mg/ml (+)-isomer stimulated the accumulation of triglyceride induced by insulin, but the addition of the same concentration of (-)-isomer inhibited lipogenesis. The activities of glycerophosphate dehydrogenase were changed by (+)- and (-)-catechin in the same direction as the corresponding changes in triglyceride accumulation. These data suggest a biological significance of catechins, with opposite effects on lipid metabolism depending on the isomer.

The influence of pycnogenol on the glycerol released into the medium in fully differentiated 3T3-L1 cells was studied. After incubation for 2 h, pycnogenol stimulated glycerol release in a dose-dependent manner. Pretreatment with the beta-receptor antagonist, propranolol, significantly reduced pycnogenol-induced lipolysis in a dose-dependent manner. When fully differentiated 3T3-L1 cells were incubated with pycnogenol, the cyclic adenosine monophosphate content significantly increased. These data suggested that pycnogenol has strong lipolytic effects via stimulation of beta-receptor mediated activity.