Nanoencapsulation and characterisation of Hypericum perforatum for the treatment of neuropathic pain.

AIM: This work aimed to encapsulate Hypericum perforatum extract (HPE) into nanophytosomes (NPs) and assess the therapeutic efficacy of this nanocarrier in neuropathic pain induced by partial sciatic nerve ligation (PSNL). METHODS: Hydroalcoholic extract of Hypericum perforatum was prepared and encapsulated into NPs by thin layer hydration method. Particle size, zeta potential, TEM, differential scanning calorimetry (DSC), entrapment efficiency (%EE), and loading capacity (LC) of NPs were reported. The biochemical and histopathological examinations were measured in the sciatic nerve. RESULTS: Particle size, zeta potential, %EE, and LC were 104.7 ± 1.529 nm, -8.93 ± 1.71 mV, 87.23 ± 1.3%, and 53.12 ± 1.7%, respectively. TEM revealed well-formed and distinct vesicles. NPHPE (NPs of HPE) was significantly more effective than HPE in reducing PSNL-inducing pain. Antioxidant levels and sciatic nerve histology were reversed to normal with NPHPE. CONCLUSIONS: This study demonstrates that encapsulating HPE with phytosomes is an effective therapeutic approach for neuropathic pain.

Pitavastatin attenuates neuropathic pain induced by partial sciatic nerve in Wistar rats.

OBJECTIVES: Pitavastatin is a competitive HMG-CoA reductase inhibitor for lowering of cholesterol level and low density lipoprotein cholesterol. This study was designed to evaluate the effect of pitavastatin in neuropathic pain induced by partial sciatic nerve ligation along with neuronal changes in Wister rats. METHODS: Pitavastatin was started three days prior to the surgery and continued for 14 days The pain was determined by thermal hyperalgesia and cold allodynia. The biochemical changes were estimated at the end of the study. The levels of cytokines were measured using an ELISA test. Western blot analysis was used to detect levels of expression of JNK, p-JNK, ERK, p-ERK, p38MAPK, p-p38MAPK. The sciatic nerve was investigated histopathologically. KEY FINDINGS: Pitavastatin significantly ameliorated nerve pain induced by PSNL and also attenuated the biochemical changes in a dose-dependent manner. The levels of inflammatory mediators were inhibited by pitavastatin. There was significant improvement in sciatic nerve fibres histology. The levels of p-38, p-ERK, and p-JNK and their associated phosphorylated proteins were reduced after treatment with pitavastatin. CONCLUSION: The present study indicates that treatment with pitavastatin reversed the PSNL-induced neuropathy in Wister rats and may be an additional therapeutic strategy in the management of neuropathic pain.

Effect of daidzein on Parkinson disease induced by reserpine in rats

Parkinson disease is a neurodegenerative disorder characterised by the cardinal symptoms of stiffness, resting tremor, slowness (bradykinesia) and reduction of movement (hypokinesia). Involvement of oxidative damage has been reported in the pathophysiology of Parkinson disease and its related complications. The purpose of this study was to examine the effect of daidzein to quench the free radicals produced as a result of the increased oxidative stress in Parkinson disease.Parkinson disease is induced by administration of reserpine (5 mg/kg/day, i.p) for 5 consecutive days. The symptoms of PD such as tremors, akinesia and rigidity were evaluated. The effect was evaluated by assessing various behavioral parameters (grip strength and locomotor activity), biochemical parameters (lipid peroxidation, and reduced glutathione), as well as histopathological parameters in brain tissue. Daidzein (an antioxidant) was administered at the dose of 50 and 100 mg/kg, p.o. once daily for 5 days. Reserpine significantly causes tremor, rigidity, akinesia and oxidative damage which were reversed by daily administration of daidzein when compared toreserpine group. There was a significant histological improvement in the neuronal degeneration in brain tissue with daidzein. So, the results indicated the protective effect of daidzein against PD.

Pycnogenol Protects against Pentylenetetrazole-Induced Oxidative Stress and Seizures in Mice.

BACKGROUND: Epilepsy is one of the most common and severe brain disorders in the world, characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition. Oxidative stress is a biochemical state in which reactive oxygen species are generated and associated with various diseases including epilepsy. Pycnogenol, a polyphenol obtained from the pine tree and has antioxidant & anti-inflammatory activity. So, the aim of the study was to evaluate the effect of Pycnogenol on pentylenetetrazole (PTZ)-induced seizures in mice. METHODS: The mice of swiss strain each weighing 18-30g were used. Pycnogenol (50&100mg/kg) was suspended in carboxymethyl cellulose in saline and administered orally. Diazepam (1mg/kg, i.p) was used as a standard drug. The anticonvulsant effects of the drugs were measured using PTZ and cognitive behaviour was also assessed. The biochemical estimation was done by measuring Thiobarbituric acid, Superoxide dismutase, Catalase, and reduced glutathione followed by the histopathological study. RESULT: Pycnogenol 50 & 100mg/kg showed a significant increase in latency to PTZ-induced seizures, decrease in duration and frequency of convulsions compared to control animals; however, the effects were dose-dependent and were more significant at a higher dose. No impairment in cognitive functions like memory and muscle relaxant was observed following pycnogenol 50 & 100 mg/kg. The effect of Pycnogenol on biochemical parameter was found to be significant. It significantly (p<0.01) decreases the level of TBARS and increases the levels of SOD, catalase, and GSH in the brain tissue. The histopathological evaluation showed less neuronal degeneration in the brain due to PTZ-induced seizures in comparison to control group. CONCLUSION: Thus pycnogenol has a protective approach towards convulsion and can be included as an adjuvant therapy with antiepileptic drugs.

Influence of carvedilol on anticonvulsant effect of gabapentin.

The present study was performed to investigate whether or not carvedilol (a beta-adrenoreceptor antagonist) potentiates the anticonvulsive activity of gabapentin against ICES (Increasing current electroshock) and PTZ (Pentylenetetrazole) induced seizures in mice. Further the effect of combination of both the drugs on spatial working memory and locomotor activity on rotarod was also evaluated. The biochemical estimation was done by measuring the lipid peroxidation and reduced glutathione in brain tissue. The results indicate that carvedilol significantly potentiates the anticonvulsive activity of gabapentin in both the models of epilepsy. The combination of both the drugs has no effect on spatial working memory and locomotor activity. In addition carvedilol in combination with gabapentin significantly decreased the level of the lipid peroxidation and increased the level of reduced glutathione (GSH) in brain. So, the present study showed that carvedilol potentiates the anticonvulsive activity of gabapentin, which can be useful for the treatment of epilepsy in patients with hypertension.