Pycnogenol ameliorates depression-like behavior in repeated corticosterone-induced depression mice model.

Oxidative stress is considered to be a mechanism of major depression. Pycnogenol (PYC) is a natural plant extract from the bark of Pinus pinaster Aiton and has potent antioxidant activities. We studied the ameliorative effect of PYC on depression-like behavior in chronic corticosterone- (CORT-) treated mice for 20 days. After the end of the CORT treatment period, PYC (0.2 mg/mL) was orally administered in normal drinking water. Depression-like behavior was investigated by the forced swimming test. Immobility time was significantly longer by CORT exposure. When the CORT-treated mice were supplemented with PYC, immobility time was significantly shortened. Our results indicate that orally administered PYC may serve to reduce CORT-induced stress by radical scavenging activity.

Hepatoprotective effects of pycnogenol in a rat model of non-alcoholic steatohepatitis.

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.

Protective effect of Pycnogenol® on ovariectomy-induced bone loss in rats.

Pycnogenol® (PYC) is a natural plant extract from the bark of Pinus pinaster and has potent antioxidant activities. The protective effect of PYC on bone loss was studied in multiparous ovariectomized (OVX) female rats. Pycnogenol® (30 or 15 mg/kg body weight/day) was administered orally to 8-month-old OVX rats for 3 months. At the end of the experiment, bone strength was measured by a three-point bending test and bone mineral density was estimated by peripheral quantitative computed tomography. Ovariectomy significantly decreased femur bone strength and bone density. Supplementation with PYC suppressed the bone loss induced by OVX. The OVX treatment significantly increased serum osteocalcin (OC) and C-terminal telopeptide of type I collagen (CTx). Supplementation with PYC reduced the serum OC and CTx in OVX rats to a level similar to that of the sham-operated group. The results indicated that orally administered PYC can decrease the bone turnover rate in OVX rats, resulting in positive effects on the biomechanical strength of bone and bone mineral density.

Anti-inflammatory effect of enzymatic hydrolysate of corn gluten in an experimental model of colitis.

OBJECTIVES: Intestinal bacteria are thought to be involved in the initiation and perpetuation of inflammatory bowel diseases. Prebiotics (non-digestable dietary carbohydrate) have beneficial properties that alter the intestinal flora and contain glutamine-rich protein. Glutamine significantly decreases indices of inflammation. In this study, an enzymatic hydrolysate of corn gluten (EHCG) was administered by gavage to Sprague-Dawley rats fed an elemental diet to determine whether EHCG can ameliorate experi- mental colitis. METHODS: Colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid after 10 days' daily oral administration of EHCG at 100 and 300 mg/kg. Macroscopic damage was assessed using a scoring system. The mucosa homogenate was sonicated and myeloperoxidase activity and histamine levels measured. KEY FINDINGS: Treatment with EHCG significantly decreased the severity of injury and reduced myeloperoxidase activity and histamine levels in the distal colon mucosa. CONCLUSIONS: EHCG may have therapeutic benefit as a supplement in enteral nutrition for patients with inflammatory bowel diseases.

(-)-Epigallocatechin-3-gallate reduces experimental colon injury in rats by regulating macrophage and mast cell.

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.

Improved effect of Pycnogenol on impaired spatial memory function in partial androgen deficiency rat model.

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.

Pycnogenol increases the probability of the contraction state in chick embryonic cardiomyocytes, indicating inotropic effects.

The influence of pycnogenol on the probability of contraction was studied in chick cardiomyocytes. Ventricles from 9-11 day chicken embryos were cultured. After 10-11 days in culture, stable spontaneous contractions were recorded and the contraction kinetics analysed. Isoproterenol and pycnogenol increased the probability of the contraction state. After pretreatment with the beta-receptor antagonist, propranolol reduced the isoproterenol- and pycnogenol-increased probability of contraction state. These data suggested that pycnogenol has inotropic effects via stimulation of beta-receptor mediated activity.

Acceleration of lipid degradation by sericoside of Terminalia sericea roots in Fully differentiated 3T3-L1 cells.

Sericoside is a traditional herbal saponin from Terminalia sericea (Family Combretaceae). The influence of sericoside on lipolysis was studied in fully differentiated 3T3-L1 cells, and glycerol release into the cytosol and residual triglyceride were measured. The addition of sericoside stimulated glycerol release into the cytosol from deposited triglyceride in a dose- and time-dependent manner. These data suggested that sericoside has a strong lipolytic activity.

Effects of green tea catechin-induced lipolysis on cytosol glycerol content in differentiated 3T3-L1 cells.

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.

Stereospecific effects of catechin isomers on insulin induced lipogenesis in 3T3-L1 cells.

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.

Therapeutic efficacy of pycnogenol in experimental inflammatory bowel diseases.

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.

Pycnogenol stimulates lipolysis in 3t3-L1 cells via stimulation of beta-receptor mediated activity.

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.