Effect of Trilinolein on Superoxide Dismutase Activity and Left Ventricular Pressure in Isolated Rat Hearts Subjected to Hypoxia and Normoxic Perfusion

Abstract

Oxygen-derived free radicals have been implicated in the development of myocardial injury during hypoxia/reperfusion. Antioxidants can effectively inhibit the formation of free radicals and ameliorate the myocardial damage which may occur during hypoxia/reperfusion. Trilinolein is a triacylglycerol recently purified from the traditional Chinese medicinal plant Panax pseudo-ginseng. It has linoleic-acid residues as the only type of fatty acid residue in all three esterified positions of the triacyglycerol. It has been proposed that decreased endogenous superoxide dismutase (SOD) activity may contribute to free radical-mediated reperfusion injury of the ischemic myocardium. In the present study, when isolated rat hearts were subjected to hypoxia for 10, 30, 60 and 90 min without normoxic perfusion, a significant decrease in Mn-SOD activity was shown throughout the period of hypoxia, whereas the Cu·Zn-SOD activity was increased at 10 and 30 min but was not different from the baseline at 60 and 90 min of hypoxia. In rat hearts pretreated with 10^–7 mol/l trilinolein and subjected to 60 min of hypoxia without normoxic perfusion, Cu·Zn-SOD was augmented compared with baseline and compared with hearts subjected to 60 min of hypoxia without trilinolein, whereas Mn-SOD activity was still reduced compared with baseline, although less so than after 60 min of hypoxia without trilinolein. Pretreatment with trilinolein was associated with better preservation of left ventricular function during hypoxia and more rapid return to recovery during normoxic perfusion. This myocardial protective effect may be related to an antioxidant effect through potentiation of SOD, particularly Cu·Zn-SOD during hypoxia.

Downregulation of Superoxide Dismutase Activity and Gene Expression in Cultured Rat Brain Astrocytes after Incubation with Vitamin C

“…Recent evidence suggests that ROS, such as superoxide anions and hydrogen peroxide, may play a role as intracellular second messengers regulating the transcription of SOD [23]. In the previous reports from our laboratory, we found that SOD gene expression and activity also can be regulated by other antioxidants, such as catechin [21] and trilinolein [24]. These results implicated that the antioxidant effect of ascorbate in the present study may be one of the major mechanisms related to SOD changes.…”

The Inhibitory Effect of Trilinolein on Norepinephrine-Induced β-Myosin Heavy Chain Promoter Activity, Reactive Oxygen Species Generation, and Extracellular Signal-Regulated Kinase Phosphorylation in Neonatal Rat Cardiomyocytes

“…Similar to that of ·-tocopherol, trilinolein was previously reported to produce an antioxidant activity in a concentration-dependent manner [5]. In rat hearts pretreated with 0.1 ÌM trilinolein and subjected to 60 min of hypoxia, Cu,Zn-SOD activity was increased compared with baseline or with hearts subjected to 60 min of hypoxia without trilinolein [6]. In addition, it has been reported that pretreatment with trilinolein appeared to be associated with better preservation of left ventricular function during hypoxia and a more rapid return to recovery during the subsequent normoxic perfusion.…”

“…In addition, it has been reported that pretreatment with trilinolein appeared to be associated with better preservation of left ventricular function during hypoxia and a more rapid return to recovery during the subsequent normoxic perfusion. [6]. A previous study has also demonstrated that myocardial protective effect of trilinolein could be related to its antioxidant effect via potentiation of SOD, particularly Cu,Zn-SOD, during hypoxia [6].…”

“…The antioxidant effects of trilinolein produce a concentration-response curve similar to that of ·-tocopherol [5]. The myocardial protective effect of trilinolein is thought to be related to antioxidant activity through potentiation of superoxide dismutase (SOD) [6]. However, the cellular and molecular mechanisms of the protective effect of trilinolein in the heart are unknown.…”

Changes of Superoxide Dismutase in Cultured Rat Aortic Smooth Muscle Cells (A7r5) by an Incubation of Vitamin E

“…Role of OFRs in myocardial injury caused by ischemia/reperfusion is apparent [5,6]. Activation of the complement system, generation of chemotactic peptides, migration and activation of polymorphonuclear cells, OFR-induced changes of membrane and lipid, and depletions of intracellular scavengers of free radicals may be involved in reperfusion injury [7]. The involvement of a superoxide radical and oxidized lipids in vessel-wall abnormalities has also been introduced in atherogenesis [4].…”