Allium schoenoprasum L. (family Amaryllidaceae), commonly known as chives has great culinary value besides being used as ethnomedicine. This review emphasises on phytochemistry and pharmacological activities of A. schoenoprasum, and discusses the future opportunities for systematic investigations. Scientific evaluation of chives validates its traditional claims and demonstrates diverse pharmacological potential including an anti-inflammatory, anticancer, antioxidant, anthelmintic and antihypertensive. Though phytochemical studies revealed the presence of sulphur and phenolic compounds, flavonoids, saponin and steroidal glycosides yet methodical research to identify bioactive compounds is required. This review confirms the medicinal importance of A. schoenoprasum and could stimulate future research on its unexplored aspects, especially identification of bioactive compounds and related mechanisms and safety, which might develop it as a drug.
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Alzheimer’s disease (AD) is one of the major reasons for 60-80% of cases of senile dementia occurring as a result of the accumulation of plaques and tangles in the hippocampal and cortical neurons of the brain leading to neurodegeneration and cell death. The other pathological features of AD comprise of abnormal microvasculature, network abnormalities, interneuronal dysfunction, increased β-amyloid production, and reduced clearance, increased inflammatory response, elevated production of reactive oxygen species, impaired brain metabolism, hyperphosphorylation of tau, and disruption of acetylcholine signaling. Among all these pathologies, mitochondrial dysfunction (MD), regardless of being an inciting insult or a consequence of the alterations, is related to all the associated AD pathologies. Observed altered mitochondrial morphology, distribution, and movement increased oxidative stress, dysregulation of enzymes involved in mitochondrial functioning, impaired brain metabolism, and impaired mitochondrial biogenesis in AD subjects suggest the involvement of mitochondrial malfunction in the progression of AD. Various pre-clinical and clinical evidence establishing MD as a key mediator in the progression of neurodegeneration in AD are reviewed and discussed with an aim to foster future MD-based drug development research for the management of AD.
Oxidative stress is strongly implicated in the pathogenesis of stroke. Strategies using antioxidants to improve neurological functions after stroke have, thus, gained significant attention. Ocimum basilicum L. is used traditionally to treat CNS disorders. Its antioxidant capacity is well established. Our laboratory has reported protective effects of pre-treatment with O. basilicum in experimental stroke, but its curative (post-treatment) effects in ischemic stroke have not been documented. Hence, the present study was aimed to evaluate the effect of O. basilicum leaf extract (OBLE) on functional outcomes following cerebral injury in mice. Cerebral injury was induced in the experimental animals by bilateral common carotid artery occlusion (BCCAO) followed by reperfusion. OBLE treatment (200 and 400 mg/kg; orally, once daily) was given for 7 days after BCCAO. Cognitive outcomes and sensorimotor disturbances were evaluated with Morris Water Maze, Elevated Plus Maze and neurological severity score, respectively. TTC (2,3,5-triphenyltetrazolium chloride) staining was used to measure cerebral infarct size. Thiobarbituric acid reactive substances, reduced glutathione levels and superoxide dismutase activity in mice brain homogenate were estimated to elucidate the neuroprotective mechanism of OBLE. Treatment with OBLE resulted in marked improvement in memory and motor coordination. OBLE also decreased cerebral infarct size and oxidative stress in mice. The extract was standardised with respect to total phenol content; an HPLC-PDA analysis showed the presence of eight phenolic acids in OBLE. It is concluded that treatment with OBLE improves functional outcomes after ischemic stroke and this may be developed as a neuroprotective drug.
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