ß-Caryophyllene, the major constituent of copaiba oil, reduces systemic inflammation and oxidative stress in arthritic rats.

The current study investigated the action of ß-caryophyllene, the major constituent of copaiba oil, on the systemic inflammation, oxidative status, and liver cell metabolism of rats with adjuvant-induced arthritis, a model for rheumatoid arthritis. This study also compared the actions of ß-caryophyllene with those previously reported for copaiba oil on arthritic rats. For this purpose, Holtzman healthy and arthritic rats received 215 and 430 mg·kg-1 ß-caryophyllene orally once a day during 18 days. Both doses of ß-caryophyllene reduced the adjuvant-induced paw edema, swollen of lymph nodes, and number of circulating and articular leukocytes. ß-Caryophyllene, at the dose of 430 mg·kg -1 , abolished the increases of protein carbonyl groups and myeloperoxidase activity in the liver and plasma of arthritic rats and, at both doses, it restored the increased levels of reactive oxygen species and reduced glutathione in the arthritic liver. These beneficial actions were of the same extension as those of copaiba oil ( Copaifera reticulata) and, therefore, ß-caryophyllene is possibly responsible for the anti-inflammatory and antioxidant actions of the oil. Hepatic gluconeogenesis was 40% lower in arthritic rats, which also presented a reduced number of hepatocytes per liver area (-23%) associated with increased hepatocyte area (+18%) and liver weight (+50%). None of these hepatic alterations were improved by ß-caryophyllene, but not even by ibuprofen. However, unlike copaiba oil, ß-caryophyllene did not modify the hepatic morphology and metabolism of healthy rats. These results reveal that ß-caryophyllene improves the systemic inflammation and oxidative status of arthritic rats and, in addition, it was not associated with hepatotoxicity.

Copaiba Oil Decreases Oxidative Stress and Inflammation But not Colon Damage in Rats with TNBS-Induced Colitis.

BACKGROUND: TNBS-induced colitis is an experimental immunopathology in rats that shares many features with human inflammatory bowel diseases. Copaiba oleoresin is extracted from plants of the genus Copaifera and is shown to reduce inflammation. OBJECTIVE: The aim of this study was to investigate the action of copaiba oil (C. reticulata Ducke) on inflammation and oxidative status in the distal colon of colitic rats. METHODS: Acute and subchronic colitis were induced in Wistar rats by an intracolonic enema with 2,4,6-trinitrobenzenesulfonic acid (TNBS). The colonic morphology was assessed by histological analysis and the oxidative stress parameters were measured in the intestinal homogenate. The liver damage markers were measured in the plasma. Control and colitic rats were orally treated either with one single dose (acute colitis) of copaiba oil (1.15 g Kg-1) or once a day during seven days (subchronic colitis). RESULTS: The intestinal morphology was severely modified by acute and subchronic colitis, as indicated by the intramural infiltration of polymorphonuclear cells and the increased thickness of all colon layers. The levels of TBARS, protein carbonyl groups and reactive oxygen species (ROS) were increased in the intestine of colitic rats. Copaiba oil did not attenuate the inflammatory damage in acute and subchronic colitis, but it decreased the activity of myeloperoxidase, leukocyte infiltration and oxidative stress in the colon. The level of plasma bilirubin and the activity of alkaline phosphatase were both increased in treated healthy and colitic rats. CONCLUSION: Copaiba oil decreased oxidative stress and inflammation but did not prevent intestinal damage in the colon of colitic rats. The alterations of plasma markers of hepatic damage caused by the oil seem to be associated to its harmful action on the liver.

Anti-Inflammatory and Antioxidant Actions of Copaiba Oil Are Related to Liver Cell Modifications in Arthritic Rats.

The present study investigated the action of copaiba oil (Copaifera reticulata) on the systemic inflammation, oxidative status, and liver cell metabolism of rats with adjuvant-induced arthritis. The later is an experimental autoimmune pathology that shares many features with the human rheumatoid arthritis. Holtzman rats were distributed into the following groups: control (healthy) rats; control rats treated with copaiba oil at the doses of 0.58 and 1.15 g · kg-1 , arthritic rats, and arthritic rats treated with copaiba oil (0.58 and 1.15 g · kg-1 ). The oil was administrated orally once a day during 18 days after arthritis induction. Both doses of copaiba oil improved the paw edema and the dose of 0.58 mg · kg-1 improved the swollen adrenals and lymph nodes besides decreasing the plasmatic myeloperoxidase activity (-30%) of arthritic rats. Copaiba oil (1.15 g · kg-1 ) abolished the increases of protein carbonyl groups and reactive oxygen species in the liver and both doses increased the liver GSH content and the catalase activity in arthritic rats. Copaiba oil (1.15 g · kg-1 ) decreased glycolysis (-65%), glycogenolysis (-58%), and gluconeogenesis (-30%) in the liver of arthritic animals. However, gluconeogenesis was also diminished by the treatment of control rats, which presented lower body weight gain (-45%) and diminished number of hepatocytes per liver area (-20%) associated to higher liver weight (+29%) and increased hepatocyte area (+13%). The results reveal that copaiba oil presented systemic anti-inflammatory and antioxidant actions in arthritic rats. These beneficial effects, however, were counterbalanced by harmful modifications in the liver cell metabolism and morphology of healthy control rats. J. Cell. Biochem. 118: 3409-3423, 2017. © 2017 Wiley Periodicals, Inc.