Effects ofGanoderma lucidumspore powder on astrocyte expression and glutamine synthetase activity in the hippocampal region of epileptic rats***

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Abstract

BACKGROUND:

Recent studies have demonstrated that astrocyte dysfunction plays a central role in inhibiting epileptic seizures and that regulation of astrocyte function may be a new target for treatment of epilepsy.

OBJECTIVE:

To observe the effects of Ganoderma lucidum spore powder (GLSP) on astrocyte morphology and glutamine synthetase (GS) activity in the hippocampal region of epileptic rats.

DESIGN, TIME AND SETTING:

A randomized, controlled animal experiment was performed at the Function Laboratory, College of Basic Medicine, Jiamusi University between October and December 2006.

MATERIALS:

A total of 30 Sprague Dawley (SD) rats were randomized to three groups (n = 10): control, model, and GLSP. GLSP was sourced from Jiamusi Wild Ganoderma Lucidum Planting Base and prepared to 30 g/L with physiological saline before use. Pentylenetetrazol (PTZ) (10 g/L) was provided by Sigma Company, USA.

METHODS:

The control group received intraperitoneal (i.p.) and intragastric (i.g.) physiological saline. Following epilepsy induction by i.p. administration of PTZ (35 mg/kg), rats from the model and GLSP groups were ig injected with physiological saline and GLSP (300 mg/kg), respectively. Each compound was administered once per day, for a total of 28 successive days. Epileptic seizure convulsions were graded 0–5. A higher grade indicated more severe epilepsy. Only those rats showing stage 2 or higher convulsions at least 5 times successively were included in further experiments.

MAIN OUTCOME MEASURES:

Immediately after injection, seizure activity was monitored for 30 minutes to determine the latent period and seizure duration; simultaneously, astrocyte numbers and GS activity in the hippocampal region of rats with epilepsy were detected by immunohistochemistry.

RESULTS:

All 30 rats were included in the final analysis. On day 28, following PTZ administration epileptic seizures were not found in the control group. In the GLSP group, rats exhibited rhythmic head nodding or facial spasms, and the latent period was significantly longer than that of the model group (P < 0.05). In the model group, the majority of rats exhibited myoclonus or generalized convulsions, and epileptic seizure duration was slightly (but not significantly) longer than that in the GLSP group (P > 0.05). Within 2–3 minutes of PTZ injection, the model group exhibited grade 4 or 5 epileptic seizures, and the GLSP group mostly showed grade 2 or 3, and occasionally grade 4 or 5, epileptic seizures. All rats recovered within 30 minutes. The model group exhibited significantly increased astrocytes (P < 0.05), with thicker cellular processes and a higher number of cellular processes, and significantly decreased GS activity (P < 0.05) than the control group. The astrocyte count was significantly decreased but GS activity was significantly increased in the GLSP group when compared with the model group (P < 0.05); however, astrocyte appearance was similar in both groups (P < 0.05).

CONCLUSION:

GLSP can effectively inhibit astrocyte numbers and elevate GS activity in the hippocampal region of rats with epilepsy, thereby reducing epileptic seizures.

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