HERBAL MEDICINES AS NEUROPROTECTIVE AGENT: A MECHANISTIC APPROACH

Neurodegeneration refers to a condition of neuronal death occurring as a result of progressive disease of long termand is becoming a major health problem in the 21st century. Neurons degenerated are not replaced resulting in cognitive loss ,many neurodegenerative disorders, such as schizophrenia, depression, Alzheimer's Disease (AD) dementia, cerebrovascular impairment, seizure disorders, head injury, Parkinsonism. Neuroprotection refers to the strategies and possible mechanisms that are able to protect the central nervous system (CNS) against neuronal injury and neurodegenerative disorders. The past decade has witnessed an intense interest in herbal plants having long-term health promoting or medicinal qualities. Comprehensive research and discovery has demonstrated that natural products, medicinal herbs, plant extracts, and their metabolites, have great potential as neuroprotective agent. Although the precise mechanisms of action of herbal drugs have yet to be determined, some of them have been shown to exert anti-inflammatory and/or antioxidant effects. Thus the herbal plants can be a valuable source of drug against neurodegenerative disorders which will require high-throughput screening. This review will highlight the role of herbal plants and their phytoconstituents against neurodegenerative diseases and other related disorders, focusing on their mechanism of action and therapeutic potential. Keywords

EFFECT OF STREBLUS ASPER LEAVES ON LOCOMOTION, ANXIETY AND COGNITION IN RATS

Objective: The current study deals with the evaluation of neuropharmacological activities of hydroalcoholic extract of the plant Streblus asper. Methods: Hydroalcoholic extract of S. asper leaves was administered to animals at the dose of 200 and 400 mg/kg p.o., respectively. The neuropharmacological activities, namely, anxiolytic, muscle-relaxant, nootropic, and locomotor activities of hydroalcoholic extract of S. asper leaves were evaluated. The antioxidant activity of the hydroalcoholic extract of S. asper leaves was also investigated. Results: The dose 400 mg/kg p.o. of hydroalcoholic extract indicated significant variation with control group on neuropharmacological activity, especially nootropic and locomotion, whereas the mentioned dose did not show a significant effect on anxiolytic and muscle-relaxant activities. Percentage scavenging activities and inhibition concentration (IC50) were reported as 63.132 at 100 μg/ml and 35.33, respectively. Conclusion: It was found that hydroalcoholic extract of S. asper leaves can treat central nervous system disorders caused by oxidative stress

Pharmacological screening of ethanolic extract of Pithecellobium dulce for antiarthritic activity in Rats

418-424Arthritis is an inflammatory joint disorder in which cartilage of the joint is gradually lost and categorized by swelling of joints, pain, and loss of function. The present study was conducted to explore the antiarthritic activity of ethanolic extract of Pithecellobium dulce against formaldehyde induced at sub plantar region of the left hind paw during days 1 and 3 of the study period. The changes observed in paw diameter during the study period, various biochemical, and haematological parameters were monitored. The Radiographic analysis and histopathology significantly improved after treatment with test extract P. dulce (250 mg/kg, b.w., p.o.) as compared to the standard treatment with indomethacin (10 mg/kg, b.w., p.o.).The results of the current investigation concluded that ethanolic extract of P. dulce possesses significant anti-arthritic activity against formaldehyde induced arthritis model, justifying its therapeutic role in arthritic conditions. The observed antiarthritic activity may be due to the presence of phytoconstituents such as alkaloids and flavonoids. P. dulce significantly suppressed the paw oedema in formaldehyde models (P <0.001). The Histopathological and radiographic studies of joints also showed a protective effect of P. dulce

Pharmacological screening of ethanolic extract of Pithecellobium dulce for antiarthritic activity in Rats

Arthritis is an inflammatory joint disorder in which cartilage of the joint is gradually lost and categorized by swelling of joints, pain, and loss of function. The present study was conducted to explore the antiarthritic activity of ethanolic extract of Pithecellobium dulce against formaldehyde induced at sub plantar region of the left hind paw during days 1 and 3 of the study period. The changes observed in paw diameter during the study period, various biochemical, and haematological parameters were monitored. The Radiographic analysis and histopathology significantly improved after treatment with test extract P. dulce (250 mg/kg, b.w., p.o.) as compared to the standard treatment with indomethacin (10 mg/kg, b.w., p.o.).The results of the current investigation concluded that ethanolic extract of P. dulce possesses significant anti-arthritic activity against formaldehyde induced arthritis model, justifying its therapeutic role in arthritic conditions. The observed antiarthritic activity may be due to the presence of phytoconstituents such as alkaloids and flavonoids. P. dulce significantly suppressed the paw oedema in formaldehyde models (P &lt;0.001). The Histopathological and radiographic studies of joints also showed a protective effect of P. dulce

CANDESARTAN REVERSES MEMORY DEFICIT CAUSED BY COLCHICINE INDUCED CHOLINERGIC DYSFUNCTION AND OXIDATIVE STRESS

Objective: We sought to investigate the protective activity of candesartan against memory impairment, oxidative stress and cholinergic dysfunction induced by activation of the central renin-angiotensin system.Methods: Male Swiss albino mice were divided into eight groups. Group 1 received vehicle (1.0% w/v gum acacia), orally for 14 d. Group 2 received intracerebrally (i. c.) artificial cerebrospinal fluid (aCSF, the vehicle of colchicine) and treated with vehicle for 14 d. Group 3, 4 and 5 injected with i. c. colchicine in the doses of 1µg, 2µg, 3µg respectively and treated with vehicle for 14 d. Group 6 and 7 received i. c colchicine (3 µg) and treated with candesartan (0.05 and 0.1 mg/kg respectively) orally for 14 d. Group 8 received i. c colchicine (3 µg) and treated with standard drug donepezil 5 mg/kg (PO) for 14 d.Learning and memory behavior was assessed by using morris water maze. Biochemical parameters of oxidative stress and cholinergic function were estimated in the brain on day 18. Parameters of oxidative stress and cholinergic function were estimated after the completion of behavioral studiesResults: Treatment with a higher dose of colchicines (3µg/mice) caused memory deficit as shown by no significant decrease in escape latency time throughout all the sessions. Results of biochemical estimation showed a marked increase in malondialdehyde (MDA), nitrite level, reduced glutathione (GSH) level, cholinotoxic effect of colchicines has been correlated by marked decrease in acetyl cholinesterase (AChE) activity. Colchicine in a dose of 3 µg/mice has been validated. Pretreatment with candesartan in doses 0.05 and 0.1 mg/kg reverses oxidative stress which can be measured by decreased MDA, nitrite level and increased GSH level. Increased AChE activity may imply protection of cholinergic neurons hence improvement in learning and memory behavior. Conclusion: Preventive treatment with angiotensins receptor blocker, candesartan showed that memory impairment induced by colchicines may be mediated by alteration of central rennin angiotensins system and loss of cholinergic neurons. This study highlighted a number of clinical findings which support marked neuroprotection by blocked of the central AT1 receptor

Chronic Inhibition of Central Angiotensin-Converting Enzyme Ameliorates Colchicine-Induced Memory Impairment in Mice

Preclinical and clinical studies indicated involvement of the central renin-angiotensin system (RAS) in memory functions. However, the role of central angiotensin-converting enzyme (ACE) in memory function is still unclear. The present study investigated the involvement of central ACE in colchicine-induced memory impairment in the context of cholinergic function and oxidative stress. Memory impairment was induced by intracerebral colchicine administration in mice. The ACE inhibitor, perindopril (0.05 and 0.1 mg/kg/day), was administered orally for 14 days. Memory function was evaluated by the Morris water maze (MWM) test from the 14th day on after colchicine injection. Donepezil was used as a standard. Parameters of oxidative stress and cholinergic function, ACE activity in serum and the brain were estimated after the completion of behavioral studies. Colchicine caused memory impairment as revealed by no significant change in latency to reach a hidden platform in the MWM test. Furthermore, there was a significant increase in MDA, ROS, and nitrite levels with a reduction in GSH level and acetylcholinesterase (AChE) activity in the brain of colchicine-treated mice. Colchicine significantly increased brain ACE activity without affecting serum ACE. Donepezil prevented colchicine-induced memory impairment in mice. The antidementic effect of perindopril may be attributed to reduced oxidative stress and improvement in cholinergic function. Moreover, the elevated brain ACE activity was also inhibited by perindopril. The study showed that central ACE plays an important role in colchicine-induced memory deficit, corroborating a number of studies that show that treatment with ACE inhibitors could be neuroprotective