Mangiferin prevents corticosterone-induced behavioural deficits via alleviation of oxido-nitrosative stress and down-regulation of indoleamine 2,3-dioxygenase (IDO) activity.

BACKGROUND: In recent years, a substantial amount of experimental studies have demonstrated that exogenous administration of corticosterone causes anxiety and depressive-like behaviour in rodents which involves hypothalamic-pituitary-adrenal axis dysregulation. Our present study aimed to explore the neuroprotective potential of mangiferin against corticosterone-induced anxiety and depressive-like behaviour. METHODS: Corticosterone (40 mg/kg; subcutaneously) was administered once daily in swiss albino mice for 21 days. Mice were treated simultaneously with mangiferin (40 mg/kg; p.o.), 30 min prior to the corticosterone injection. RESULTS: Chronic administration of corticosterone caused anxiety and depressive-like behaviour in mice which was significantly alleviated by mangiferin treatment. Biochemical analysis revealed that mangiferin treatment significantly attenuated corticosterone-induced oxido-nitrosative stress and neuroinflammation in the hippocampus region. Furthermore, concomitant treatment with mangiferin significantly enhanced the hippocampal brain-derived neurotrophic factor (BDNF) level and decreased the serum corticosterone level in the corticosterone-treated animals. Western blotting analysis revealed that corticosterone administration significantly up-regulated the indoleamine 2,3-dioxygenase (IDO) protein expression level in the hippocampus which was significantly reduced by mangiferin treatment. CONCLUSION: Taken together, our results suggest that mangiferin exerts anti-anxiety and antidepressant effect in corticosterone-treated rats, which is probably mediated through up-regulation of BDNF level along with inhibition of oxido-nitrosative stress, neuroinflammation and IDO up-regulation in the hippocampus region.

Antinociceptive effects of endomorphin-2: suppression of substance P release in the inflammatory pain model rat.

Endomorphin-2 (EM2) and Substance P (SP) exert suppressive and facilitative influences upon nociception, respectively. Although EM2 and SP were often co-expressed in single neurons in dorsal root ganglion (DRG), it is still unknown if and how the nociception-suppressive influences of EM2 might be exerted upon nociception-facilitative effects of SP in the DRG neurons. We examined these issues in the inflammatory pain model rats produced by subcutaneous injection of the complete Freund's adjuvant into the hind paw. The paw withdrawal threshold for mechanical allodynia was measured. Changes of EM2 and SP release were estimated by measuring intrathecal levels of EM2 and SP through in vivo microdialysis analysis of cerebrospinal fluid. The mechanical allodynia was dose-dependently attenuated by intrathecal injection of EM2 or a neurokinin-1 receptor antagonist, and facilitated by intrathecal injection of SP or a mu-opioid receptor (MOR) antagonist. Importantly, intrathecal level of SP was found to be lowered by intrathecal injection of EM2. Morphologically, colocalization of EM2-, MOR- and SP-immunoreactivity in single DRG neurons was observed by immunofluorescent histochemistry, and co-expression of EM2 and SP in large, dense-cored presynaptic vesicles in primary afferents, as well as localization of MOR on pre- and postsynaptic membrane in spinal dorsal horn, was also confirmed electron miscroscopically. Thus, the results indicated that analgesic influences of EM2 upon inflammatory pain might be exerted through suppression of SP release, supporting the assumptions that binding of EM2 to presynaptic MOR might induce such effects.

[Effect of radiofrequency of different temperatures and durations on motor conduction velocity of rat sciatic nerve].

OBJECTIVE: To evaluate the effect of radiofrequency of different temperatures and durations on sciatic nerve motor conduction velocity (MCV). METHODS: The bilateral sciatic nerve of 70 adult SD rats was dissected and exposed to radiofrequency ablation of different temperatures (30, 50, 55, 60, and 70 degrees C) and durations. The nerves were also exposed to increasing ablation temperatures from 30 degrees C to 50 degrees C with an increment of 5 degrees C (60 s at each temperature), and the changes in the MCV parameters were observed. RESULTS: The MCV parameters of rat sciatic nerve underwent significant changes following the radiofrequency exposures (P<0.05) except for the exposure at 55 degrees celsius; for 10 s. Below the temperature of 55 degrees celsius;, the MCV showed no obvious correlation to the exposure time for the group. For the nerves exposed to radiofrequency of 55 degrees celsius;, the latency was not correlated to the exposure time within 30 s, and data could be obtained from 55 s group; with these exceptions, the latency was found to positively while the negative phase wave inversely correlated to the exposure time. With fixed exposure time of 60 s, the MCV parameters were positively correlated to the ablation temperature (below 50 degrees C). Failure of MCV measurement occurred following exposures to 55 degrees celsius; for 50 s (or longer) or to 60 degrees C (or higher) for 10 s. CONCLUSION: Low-temperature radiofrequency (below 50 degrees C) produces definite effects on the MCV of rat sciatic nerve, and the effects are not associated with the exposure time, the mechanism of which remains unclear. At a given temperature, the ablation for sufficiently long durations can result in complete block of the MCV. At higher temperatures, radiofrequency exposure cause obvious nerve conduction block.