Coadministration of dexamethasone and melissa officinalis has neuroprotective effects in rat animal model with spinal cord injury

Objective: Spinal cord injury [SCI] causes inflammation, deformity and cell loss. It has been shown that Melissa officinalis [MO], as herbal medicine, and dexamethasone [DEX] are useful in the prevention of various neurological diseases. The present study evaluated combinational effects of DEX and MO on spinal cord injury

Materials and Methods: Thirty six adult male Wistar rats were used in this experimental study. The weight-drop contusion method was employed to induce spinal cord injury in rats. DEX and MO were administrated alone and together in different treatment groups. Intra-muscular injection of DEX [1 mg/kg] was started three hours after injury and continued once a day for seven days after injury. Intra-peritoneal [I.P] injection of MO [150 mg/ kg] was started one day after injury and continued once a day for 14 days

Results: Our results showed motor and sensory functions were improved significantly in the group received a combination of DEX and MO, compared to spinal cord injury group. Mean cavity area was decreased and loss of lower motor neurons and astrogliosis in the ventral horn of spinal cord was significantly prevented in the group received combination of DEX and Melissa officinalis, compared to spinal cord injury group. Furthermore, the findings showed a significant augmentation of electromyography [EMG] recruitment index, increase of myelin diameter, and up-regulation of myelin basic protein in the treated group with combination of DEX and MO

Conclusion: Results showed that combination of DEX and MO could be considered as a neuroprotective agent in spinal cord injury

Chronic intracerebroventricular administration of dimethyl sulfoxide attenuates streptozotocin-iduced memory loss in rats

The memory impairment, obtained from intracerebroventricular [i.c.v.] infusion of streptozotocin in rats through activation of oxidative stress, is accepted as sporadic Alzheimer's disease model in most experimental studies. Dimethyl sulfoxide [DMSO] as a solvent is widely used in animal studies to have antioxidant effects as well. However, no report is available about DMSO effect on oxidative stress-induced cognition deficit i.e. Alzheimer's disease. The present work was designed to assess the effect of chronic treatment of DMSO on STZ-treated rats. STZ [3 mg/ kg; i.c.v.; bilateral with 10 micro l volume in either side; days 1 and 3] using a single-day version of Morris water maze. The DMSO [2.5, 5 and 10%v/v in saline], started from the first day, was infused for 14 days. The chronic administration of DMSO 10% improved the distance to hidden platform [P<0.01] in training sessions and time spent in the target quadrant in probe tests [P<0.01]. Neither STZ nor DMSO had any intervention on velocity and visuo-motor coordination in the visible version of MWM. Totally, the results suggest that DMSO may be appropriate as adjuvant therapies for the prevention of memory impairment in the experimental models of Alzheimer's disease. Therefore, use of DMSO as a solvent in Alzheimer's disease animal studies should be considered having beneficial effects on cognitive function