Abstract
Ursolic acid (UA) is a plant derived compound which is also a component of the standard human diet. It possesses a wide range of pharmacological properties, i.e., antioxidant, anti-inflammatory, antimicrobial and antitumor, which have been used in folk medicine for centuries. Moreover, influence of UA on central nervous system-related processes, i.e., pain, anxiety and depression, was proved in experimental studies. UA also revealed anticonvulsant properties in animal models of epilepsy and seizures. The aim of the present study was to investigate the influence of UA on seizure thresholds in three acute seizure models in mice, i.e., the 6 Hz-induced psychomotor seizure threshold test, the maximal electroshock threshold (MEST) test and the timed intravenous pentylenetetrazole (iv PTZ) infusion test. We also examined its effect on the muscular strength (assessed in the grip strength test) and motor coordination (estimated in the chimney test) in mice. UA at doses of 50 and 100 mg/kg significantly increased the seizure thresholds in the 6 Hz and MEST tests. The studied compound did not influence the seizure thresholds in the iv PTZ test. Moreover, UA did not affect the motor coordination and muscular strength in mice. UA displays only a weak anticonvulsant potential which is dependent on the used seizure model.
Highlights
Throughout the ages plants and their extracts were used as remedies for a wide range of disorders
In order to verify the reliability of the seizure tests, we evaluated the influence of sodium valproate (VPA, at a dose of 150 mg/kg in the intravenous pentylenetetrazole (iv PTZ) and maximal electroshock threshold (MEST) tests and at a dose of 50 mg/kg in the 6 Hz test) on seizure thresholds
Seizure threshold in the control group was 11.57 (11.01–12.06) mA while in group which was injected with Ursolic acid (UA) at a dose of 50 mg/kg it was raised by ~15% (p < 0.05 vs. negative control group)
Summary
Throughout the ages plants and their extracts were used as remedies for a wide range of disorders. Experimental studies revealed that UA might be used for the prevention/treatment of Parkinson’s disease because it showed a number of neuroprotective properties in animals treated with 1-methyl-4-phenyl-1,2,3,6-tetra hydropyridine [13]. The ability of UA to block the p38/NF-κB signaling pathways [14] and Forkhead box protein O1 as well as to activate PI3K/Akt signaling [15] might attenuate cognitive deficits in experimental models. Liang et al [16] showed that UA significantly reduced the amyloid β-induced learning and memory deficits in mice through reduction of oxidative stress and inflammatory response, which implies that this triterpenoid may offer a novel therapeutic strategy for the treatment of Alzheimer’s disease [16]. A potent mechanism for its neuroprotective effects in mice after middle cerebral artery occlusion is upregulation of the nuclear factor-erythroid 2-related factor 2 pathway [17]
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