Alpha linolenic acid in maternal diet halts the lipid disarray due to saturated fatty acids in the liver of mice offspring at weaning.

Background: Alpha linolenic acid (ALA, 18:3) in maternal diets has been shown to attenuate obesity associated insulin resistance (IR) in adult offspring in mice. The objective in the present study was to detect the early effects of maternal dietary saturated fatty acids (SFA) and their partial substitution with ω-3 ALA, docosa hexenoic acid (DHA,22:6) and eicosapentenoic acid 20:5 (EPA,20:5) on the HOMA index, liver lipids and fatty acid desaturases in the offspring at weaning.

Methods: 3 month old C57Bl6/J female mice were fed diets containing normal amount of calories but rich in SFA alone or partially replaced with ALA, DHA or EPA before mating, during pregnancy and lactation.

Perioperative use of beta-blockers and COX-2 inhibitors may improve immune competence and reduce the risk of tumor metastasis.

Background: COX inhibitors and beta-blockers were recently suggested to reduce cancer progression through inhibition of tumor proliferation and growth factor secretion, induction of tumor apoptosis, and prevention of cellular immune suppression during the critical perioperative period. Here we evaluated the perioperative impact of clinically applicable drugs from these categories in the context of surgery, studying natural killer (NK) cell activity and resistance to experimental metastases.

Methods: F344 rats were treated with COX-1 inhibitors (SC560), COX-2 inhibitors (indomethacin, etodolac, or celecoxib), a beta-blocker (propranolol), or a combination of a COX-2 inhibitor and a beta-blocker (etodolac and propranolol).

A tale of switched functions: from cyclooxygenase inhibition to M-channel modulation in new diphenylamine derivatives.

Cyclooxygenase (COX) enzymes are molecular targets of nonsteroidal anti-inflammatory drugs (NSAIDs), the most used medication worldwide. However, the COX enzymes are not the sole molecular targets of NSAIDs. Recently, we showed that two NSAIDs, diclofenac and meclofenamate, also act as openers of Kv7.

Nutritional-pharmacological combinations--a novel approach to reducing colon cancer incidence.

Background: Recent studies have suggested that n-9 fatty acids in olive oil prevent colon carcinogenesis while n-6 PUFA seems to activate this process.

Aims: To evaluate the effects of nutritional-pharmacological combinations made up of olive or soy oil-based diets and the drug sulindac, on colon cancer incidence in a chemically induced (1,2-dimethylhydrazine, DMH) rat cancer model.

Methods: Male rats were assigned to two different dietary regimes based on a standard murine defined diet (AIN-76A) containing either a low (4%) or high (15 %) concentration of olive or soy oil.

Differential metabolism of dihomo-gamma-linolenic acid and arachidonic acid by cyclo-oxygenase-1 and cyclo-oxygenase-2: implications for cellular synthesis of prostaglandin E1 and prostaglandin E2.

Prostaglandin (PG) E(1) has been shown to possess anti-inflammatory properties and to modulate vascular reactivity. These activities are sometimes distinct from those of PGE(2), suggesting that endogenously produced PGE(1) may have some beneficial therapeutic effects compared with PGE(2). Increasing the endogenous formation of PGE(1) requires optimization of two separate processes, namely, enrichment of cellular lipids with dihomo-gamma-linolenic acid (20:3 n-6; DGLA) and effective cyclo-oxygenase-dependent oxygenation of substrate DGLA relative to arachidonic acid (AA; 20:4 n-6).

Is inhibition of cyclooxygenase required for the anti-tumorigenic effects of nonsteroidal, anti-inflammatory drugs (NSAIDs)? In vitro versus in vivo results and the relevance for the prevention and treatment of cancer.

Active research is being conducted to unravel the cellular mechanisms mediating the anti-tumorigenic effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and their association with cyclooxygenase (COX) inhibition. The majority of NSAIDs inhibit either COX-1, COX-2, or both and exert their anti-COX, anti-inflammatory, and anti-tumorigenic effects in vivo in a parallel dose-dependent manner. The effects are seen at NSAID blood plasma concentrations of 0.