Attenuated Renal and Hepatic Cells Apoptosis Following Swimming Exercise Supplemented with Garlic Extract in Old Rats.

BACKGROUND/OBJECTIVE: One of the problems associated with aging is the development of apoptosis in different tissues. There is evidence that physical activity and herbal remedies can be useful. This study aimed to determine the effect of swimming training (SW) alone or combined with garlic extract on renal and hepatic cells apoptosis, as wellas on the liver and kidney function biomarkers in old rats. METHODS: A total of 35 old rats (aged 40-50 weeks) were randomly divided into 5 groups including control, saline (S), exercise training (ET), garlic (G) and exercise training+ garlic (ET.G) groups. Exercise was started for 5 min/day and then gradually extended to 60 min/day and the G and E+G groups received 1 mL/kg of this mixture by gavage. Twenty-four hours after completion of 8 weeks training, liver, kidney and blood samples were collected for histopathological examinations, liver and kidney functions, oxidative stress and apoptosis biomarkers. RESULTS: The tissue sections of the SW exercise, control and saline groups showed some mild histopathological changes in liver and kidney, while SW supplemented with garlic prevented these damages. The SW alone or supplemented with garlic significantly increased the Bcl-2 value and declined the BAX level in both liver and kidney (p<0.05). The activities of catalase (CAT) and superoxide dismutase (SOD) in the liver and kidney of the control and saline groups were lower than those in E, G and G+E groups, while a significant increase for malondialdehyde (MDA) value was found in the control and saline groups. Furthermore, the E+G significantly declined the activity of hepatic (ALT, AST and ALP) and renal damage (uric acid, urea and creatinine) biomarkers compared to the control and saline groups (p<0.05). DISCUSSION: Swimming exercise supplemented with garlic extract not only improves antioxidant capacity but also declines oxidative damages and apoptosis through reducing Bax levels and enhancing Bcl-2 value.

On the mechanism of carbamazepine-induced antinociception in the formalin test.

In the present study, the effect of lidocaine (a sodium channel blocker) on carbamazepine-induced antinociception, in formalin test was investigated. Intraperitoneal (i.p.) administration of different doses of carbamazepine (3.5, 7, 15, and 30 mg/kg) induced a dose-dependent antinociception in mice, in the first and second phases of the test. Different doses of lidocaine as a sodium channel blocker (5, 10, and 20 mg/kg, i.p.) also induced antinociception in both phases of the formalin test. It is noted that lidocaine could potentiate the response of carbamazepine in the first, but not in the second, phase of the formalin test. Meanwhile i.p. administration of different doses of Prazosin, alpha1 adrenoceptor antagonist (0.125, 0.25, and 0.5 mg/kg), Yohimbine, alpha2 adrenoceptor antagonist (0.25, 0.5, and 1 mg/kg), Bicuculline, GABAA receptor antagonist (1.5 and 3 mg/kg), and CGP 35348, GABAB receptor antagonist (100 and 200 mg/kg) exert dose-dependent antinociceptive effect in both phases of the formalin test. It should be noted that bicuculline 0.75 mg/kg by itself increased pain score in the second phase of the formalin test, indicating that blockade of GABAA receptor subtype may induce chronic pain. None of the aforementioned drugs could alter the antinociceptive response of carbamazepine in the formalin test. It is concluded that sodium channel mechanisms may be involved partly in the antinociceptive induced by carbamazepine.