Leonurine Protects Middle Cerebral Artery Occluded Rats Through Antioxidant Effect and Regulation of Mitochondrial Function

Abstract

Background and Purpose-Oxidative stress is known to be involved in ischemic stroke. Intense interest is drawn to the therapeutic potential of Chinese herbs on ischemic stroke because many of them contain antioxidant properties. Leonurine, 1 of the active compounds from purified Herba Leonuri, was studied to evaluate its possible therapeutic effects on ischemic stroke. Method-Middle cerebral artery occlusion was selected as our model of study. The animals were pretreated with Leonurine orally for 7 days and the surgery was done. One day after surgery, 2,3,5-triphenyltetrazolium chloride staining and neurological deficit score were carried out to evaluate the functional outcome of animals, whereas levels of superoxide dismutase, glutathione peroxidase, and malondialdehyde were analyzed for oxidative stress analysis. For mitochondrial studies, 3 hours after surgery, mitochondria were isolated for analysis of reactive oxygen species production, adenosine triphosphate biosynthesis, oxygen consumption, and respiratory control ratio value. Result-In in vivo experiments, Leonurine pretreatment reduced infarct volume, improved neurological deficit in stroke groups, increased activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase, and decreased levels from the lipid peroxidation marker malondialdehyde. In terms of mitochondrial modulation, Leonurine inhibited mitochondrial reactive oxygen species production and adenosine triphosphate biosynthesis. Animal studies also demonstrated that the mitochondrial function and redox state were restored by Leonurine treatment. Conclusions-Leonurine has neuroprotective effects and carries a therapeutic potential of stroke prevention. (Stroke.

Perfluorooctanoic acid exposure alters polyunsaturated fatty acid composition, induces oxidative stress and activates the AKT/AMPK pathway in mouse epididymis

“…The protein concentration of the supernatant was measured using the BCA method. The detections of superoxide dismutase (SOD), malonaldehyde (MDA), and glutathione peroxidase (GSH-Px) were performed via the nitroblue tetrazolium-illumination method, thiobarbituric acid method, and benzoic acid method, respectively (Loh et al, 2010;Liu et al, 2013;Zhang et al, 2014b) using commercially available kits (Nanjing Jiancheng Bioengineering Institute, Nanjing, China).…”

Effects of <i>Leonurine</i> on L-Type Calcium Channel in Rat Ventricular Myocytes

“…6) Using middle cerebral artery occlusion model we also found Leo had neuroprotective effects. 7) The antioxidative and anti-apoptotic effects were, at least in part, involved in the underlying mechanism. But other mechanisms remain elusive.…”

“…13) Our previous studies have shown that Leo decreased intracellular Ca 2+ 3,4) and exerted mitochondrial protective effect both in cardiomyocytes and brain. 3,7) But little was known about the mechanism underlying this phenomenon.…”

Leonurine Prevents Atherosclerosis Via Promoting the Expression of ABCA1 and ABCG1 in a Pparγ/Lxrα Signaling Pathway-Dependent Manner

“…A large body of evidence has indicated that leonurine is effective in preventing many disorders through many ways, including stoke [36], chronic myocardial infarction [16, 37] and acute kidney injury [38]. Yuan et al [39] found that leonurine hydrochloride (LH), an artificial chemical compound sharing the similar structure of leonurine, can protect against osteoclast-related diseases via inhibiting receptor activator NF-κB ligand (RANKL)-TNF receptor-associated factor 6 (TRAF6) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways.…”