Glycemic homeostasis and hepatic metabolism are modified in rats with global cerebral ischemia.

Cerebral ischemia-induced hyperglycemia has been reported to accentuate neurological damage following focal or global cerebral ischemia. Hyperglycemia found in rats following focal brain ischemia occurs in the first 24 h and has been claimed to be caused by increased liver gluconeogenesis and insulin resistance. However, liver gluconeogenesis and the mechanisms leading to hyperglycemia after global cerebral ischemia remain uncertain. This study investigated the glycemic homeostasis and hepatic metabolism in rats after transient four-vessel occlusion (4-VO)-induced global cerebral ischemia, an event that mimics to a certain degree the situation during cardiac arrest. Several metabolic fluxes were measured in perfused livers. Activities and mRNA expressions of hepatic glycolysis and glyconeogenesis rate-limiting enzymes were assessed as well as respiratory activity of hepatic isolated mitochondria. Global cerebral ischemia was associated with hyperglycemia and hyperinsulinemia 24 h after ischemia. Insulin resistance developed later and was prominent after the 5th day. Hepatic anabolism and catabolism were both modified in a complex and time-dependent way. Gluconeogenesis, ß-oxidation, ketogenesis and glycolysis were diminished at 24 h after ischemia. At 5 days after ischemia glycolysis had normalized, but gluconeogenesis, ketogenesis and ß-oxidation were accelerated. The overall metabolic modifications suggest that a condition of depressed metabolism was established in response to the new conditions generated by the cerebral global ischemia. Whether the modifications in the liver metabolism found in rats after the ischemic insult can be translated to individuals following global brain ischemia remains uncertain, but the results of this study are hoped to encourage further investigations.

Methyl Jasmonate Reduces Inflammation and Oxidative Stress in the Brain of Arthritic Rats.

Methyl jasmonate (MeJA), common in the plant kingdom, is capable of reducing articular and hepatic inflammation and oxidative stress in adjuvant-induced arthritic rats. This study investigated the actions of orally administered MeJA (75-300 mg/kg) on inflammation, oxidative stress and selected enzyme activities in the brain of Holtzman rats with adjuvant-induced arthritis. MeJA prevented the arthritis-induced increased levels of nitrites, nitrates, lipid peroxides, protein carbonyls and reactive oxygen species (ROS). It also prevented the enhanced activities of myeloperoxidase and xanthine oxidase. Conversely, the diminished catalase and superoxide dismutase activities and glutathione (GSH) levels caused by arthritis were totally or partially prevented. Furthermore, MeJA increased the activity of the mitochondrial isocitrate dehydrogenase, which helps to supply NADPH for the mitochondrial glutathione cycle, possibly contributing to the partial recovery of the GSH/oxidized glutathione (GSSG) ratio. These positive actions on the antioxidant defenses may counterbalance the effects of MeJA as enhancer of ROS production in the mitochondrial respiratory chain. A negative effect of MeJA is the detachment of hexokinase from the mitochondria, which can potentially impair glucose phosphorylation and metabolism. In overall terms, however, it can be concluded that MeJA attenuates to a considerable extent the negative effects caused by arthritis in terms of inflammation and oxidative stress.

Effects of in vitro gastrointestinal digestion and colonic fermentation on a rosemary (Rosmarinus officinalis L) extract rich in rosmarinic acid.

The potential phytochemical losses occurring throughout the sequential steps of in-vitro gastrointestinal digestion and colonic fermentation of a rosemary aqueous extract were investigated. Crude (CE), digested (DE) and fermented (FE) extracts were characterized in terms of their phenolic profile and biological activities. Rosmarinic acid was the phytochemical that underwent the most significate transformation during digestion and fermentation, which amounted to 60% compared to the 26% degradation of the total phenolics. Overall, the simulated digestion step decreased the antioxidant activity estimated by DPPH, ABTS, FRAP, ORAC and TBARS assays. Both CE and DE did not present antiproliferative potential, however, FE exhibited a pronounced cytotoxic activity (GI50 = 116 µg/mL) against HeLa cells. CE and DE showed to be moderate inhibitors of methicillin-resistant Staphylococcus aureus (MRSA), methicillin-susceptible S. aureus (MSSA), S. aureus, Listeria monocytogenes, whilst the FE acted as a moderate inhibitor of MRSA and MSSA.

Anti-Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats.

Methyl jasmonate (MeJA) is a fatty acid-derived cyclopentanone which shares structural similarities with prostaglandins and has been under study as a promising anti-inflammatory agent. This study investigated the actions of MeJA on systemic inflammation and oxidative status in rats with adjuvant-induced arthritis, a model for rheumatoid arthritis. MeJA (75 to 300 mg·kg-1) was administrated orally during 18 days after arthritis induction with Freund's adjuvant. Articular and systemic inflammation was greatly increased in arthritic rats, likewise the oxidative stress in plasma and liver. The hepatic glucokinase activity and glycolysis were increased in arthritic rats. MeJA decreased most inflammatory parameters and abolished the increased protein carbonylation in plasma and liver, diminished the increased hepatic ROS content, and restored the hepatic GSH/GSSG ratio in arthritic rats. However, the MeJA treatment decreased the hepatic glucokinase activity and glycolysis and stimulated mitochondrial ROS production in healthy and arthritic rats. Oxygen uptake was increased by MeJA only in livers from treated arthritic rats. This action may bear relation to the increased activity of mitochondrial NADP+-dependent enzymes to provide reducing equivalents for the glutathione cycle. These beneficial effects, however, are associated with a decreased glucose flux through the glycolysis in the liver of arthritic and healthy rats.

Effects of in vitro digestion and in vitro colonic fermentation on stability and functional properties of yerba mate (Ilex paraguariensis A. St. Hil.) beverages.

Yerba mate (Ilex paraguariensis) is a plant that grows naturally in South America. From its leaves and thin stems different kinds of beverages are prepared (chimarrão, tererê and tea mate), all of them rich in bioactive substances. The aim of this study was to evaluate the influence of in vitro gastrointestinal digestion and colonic fermentation on the stability of the polyphenols and on the antioxidant, antimicrobial and antitumoral activities of the yerba mate beverages. The phenolic chromatographic profile revealed that both the in vitro digestion and the colonic fermentation caused a pronounced decrease in 3,5-O-dicaffeoylquinic acid and 5-O-caffeoylquinic acid in the preparations. However, 3-O-caffeoylquinic acid, 4-O-caffeoylquinic acid and salvianolic acid I were only barely affected in all preparations. Despite the decrease in the phytochemicals content, yerba mate beverages maintain their functional properties such as antioxidant, antibacterial and antitumoral activities.