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  • Bentham Science Publishers Ltd.  (3)
  • English  (3)
  • 1
    In: Current Pharmaceutical Design, Bentham Science Publishers Ltd., Vol. 26, No. 34 ( 2020-10-13), p. 4234-4245
    Abstract: Inflammation is a devastating outcome of cerebrovascular diseases (CVD), namely stroke and atherosclerosis. Numerous studies over the decade have shown that inflammasomes play a role in mediating inflammatory reactions post cellular injury occurring after a stroke or a rupture of an atherosclerotic plaque. In view of this, targeting these inflammatory pathways using different pharmacological therapies may improve outcomes in patients with CVD. Here, we review the mechanisms by which inflammasomes drive the pathogenesis of stroke and atherosclerosis. Also, discussed here are the possible treatment strategies available for inhibiting inflammasomes or their up-stream/down-stream mediators.
    Type of Medium: Online Resource
    ISSN: 1381-6128
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2020
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Bentham Science Publishers Ltd. ; 2020
    In:  Current Topics in Medicinal Chemistry Vol. 20, No. 13 ( 2020-06-09), p. 1154-1168
    In: Current Topics in Medicinal Chemistry, Bentham Science Publishers Ltd., Vol. 20, No. 13 ( 2020-06-09), p. 1154-1168
    Abstract: The occurrence of secondary neurodegeneration has exclusively been observed after the first incidence of stroke. In humans and rodents, post-stroke secondary neurodegeneration (SND) is an inevitable event that can lead to progressive neuronal loss at a region distant to initial infarct. SND can lead to cognitive and motor function impairment, finally causing dementia. The exact pathophysiology of the event is yet to be explored. It is seen that the thalami, in particular, are susceptible to cause SND. The reason behind this is because the thalamus functioning as the relay center and is positioned as an interlocked structure with direct synaptic signaling connection with the cortex. As SND proceeds, accumulation of misfolded proteins and microglial activation are seen in the thalamus. This leads to increased neuronal loss and worsening of functional and cognitive impairment. Objective: There is a necessity of specific interventions to prevent post-stroke SND, which are not properly investigated to date owing to sparsely reproducible pre-clinical and clinical data. The basis of this review is to investigate about post-stroke SND and its updated treatment approaches carefully. Methods: Our article presents a detailed survey of advances in studies on stroke-induced secondary neurodegeneration (SND) and its treatment. Results: This article aims to put forward the pathophysiology of SND. We have also tabulated the latest treatment approaches along with different neuroimaging systems that will be helpful for future reference to explore. Conclusion: In this article, we have reviewed the available reports on SND pathophysiology, detection techniques, and possible treatment modalities that have not been attempted to date.
    Type of Medium: Online Resource
    ISSN: 1568-0266
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2020
    SSG: 15,3
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Bentham Science Publishers Ltd. ; 2022
    In:  Central Nervous System Agents in Medicinal Chemistry Vol. 22, No. 3 ( 2022-12), p. 175-187
    In: Central Nervous System Agents in Medicinal Chemistry, Bentham Science Publishers Ltd., Vol. 22, No. 3 ( 2022-12), p. 175-187
    Abstract: Ischemic stroke remains the leading cause of death worldwide and is the primary cause of disability globally. Numerous studies have shown that plant-origin medicines are promising and can influence the treatment of neurological disorders. Phyllanthus embilica L. (P. emblica or Amla) is one of the herbal plants whose medicinal properties are widely studied. The objective of the present study is to determine the neuroprotective effects of an aqueous extract of the fruit of P. emblica (hereinafter referred to as just P. emblica) on cerebral ischemia-reperfusion injury and explore if it can regulate BDNF/PI3K pathway to modulate glutathione for mitoprotection and neuroprotection. Methods: In vivo studies were conducted on male Sprague Dawley rats, where rats were prophylactically administered 100 mg/kg P. emblica for 30 days. In the treatment group, rats were given 100 mg/kg P. emblica, 1 h post middle cerebral artery occlusion (MCAo). Rats were evaluated for neuro deficit and motor function tests. Brains were further harvested for infarct size evaluation, biochemical analysis, protein expression studies, and mitochondrial studies. Results: Prophylaxis and treatment with P. emblica demonstrated significant improvement in functional outcome with a reduction in infarct size. Normalization of glutathione, nitrite, and malondialdehyde levels was also observed. Improvement in mitochondrial complex I and IV activities was also reported. Expressions of BDNF, PI3K, SDF1 and VEGF increased while that of ROCK2 decreased following P. emblica administration. Conclusion: P. emblica regulates BDNF/PI3K pathway to modulate glutathione in ischemic stroke to confer mitoprotection and neuroprotection.
    Type of Medium: Online Resource
    ISSN: 1871-5249
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2022
    SSG: 15,3
    Location Call Number Limitation Availability
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