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Diabetic neuropathy (DN) is the highly occurred complication of diabetes mellitus; it has been defined as an event of peripheral nerve dysfunction characterized by pain, allodynia, hyperalgesia, and paraesthesia. The current study was conducted to evaluate the efficacy of low-level laser therapy (LLLT) in the management of neuropathy in diabetic rats. The used animals were divided into the following groups: negative control, streptozotocin-induced diabetic rats, and diabetic rats with peripheral neuropathy (DNP) and DNP treated with gabapentin or with LLLT. Behavioral tests were carried out through hotplate test for the determination of pain sensations and the Morris water maze test for spatial reference memory evaluation. Blood samples were collected at the end of treatment for biochemical determinations. In the current study, the latency of hind-paw lick decreased significantly when DNP are treated with gabapentin or LLLT. The Morris water maze test showed that LLLT treatment improved memory that deteriorated in DNP more than gabapentin do. The results of the biochemical study revealed that LLLT could not affect the level of beta-endorphin that decreased in DNP but significantly decreased S100B that rose in DNP. PGE2 and cytokines IL-1β, IL-10, and TNF-α showed significant increase in DNP compared with control group. The gabapentin administration or LLLT application significantly reversed the levels of the mentioned markers towards the normal values of the controls. Levels of serum MDA and nitric oxide increased significantly in the DNP but rGSH showed significant decrease. These markers were improved significantly when the DNP were treated with gabapentin or LLLT. The treatment with gabapentin or LLLT significantly decreased the raised level in total cholesterol in DNP but could not decrease the elevated level of triglycerides, while LDL cholesterol decreased significantly in DNP treated with gabapentin but not affected by LLLT. Values of serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), urea, and creatinine increased significantly in the DPN and diabetic rats without peripheral neuropathy (PN) compared with control group. The treatment of DNP with gabapentin induced significant increases in ALAT and ASAT activities but LLLT treatment induced significant decreases in ALAT and ASAT activities as compared with DNP group. Neither gabapentin nor LLLT could improve the elevated levels of serum urea and creatinine in the DNP. It could be concluded that LLLT is more safe and effective than gabapentin in the management of neuropathy in diabetic rats.

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Objective: The present objective is to evaluate the antidepressant activity of caffeine. Material and methods: Three groups of rats were used; control, reserpine-induced rat model of depression, and rat model of depression treated daily with caffeine. At the end of the experiment, the motor activity of rats was measured using open field test. On the next day, the animals of the three groups were sacrificed to measure levels of serotonin, norepinephrine, and dopamine in the cortex and hippocampus by spectrofluorometer. In addition, the levels of lipid peroxidation (MDA), nitric oxide (NO), and reduced glutathione (GSH) together with the activities of acetylcholinesterase (AchE) and Na + , K + , ATPase were measured in the two studied brain regions by spectrophotometer. Results: In the rat model of depression, the animals showed a significant decrease in motor activity. This was associated with significant decreases in serotonin, norepinephrine, and dopamine in the cortex and hippocampus. However, significant increases in the activities of AchE and Na + , K + , ATPase, and the levels of MDA and NO were recorded in both areas of rat model of depression while GSH showed a significant decrease in the hippocampus. Caffeine failed to restore the decrease in motor activity. Caffeine treatment ameliorated the changes in cortical and hippocampal norepinephrine and dopamine and hippocampal serotonin. In addition, it restored MDA and GSH levels. However, it failed to prevent the increased AchE and Na + , K + , ATPase activities, and NO levels. Conclusions: The present findings indicate that caffeine has a partial antidepressant effect mediated by its antioxidant activity and enhancement of monoamine levels.