Evaluation and Comparison of Anticonvulsant Activity of t elmisartan and Olmesartan in Experimentally Induced Animal Models of Epilepsy

Pushpa, V H; K, Padmaja Shetty; Suresha, R N; Jayanthi, M K; Ashwini,; S, Vaibhavi P

doi:10.7860/jcdr/2014/9455.5061

Cited by 6 publications

(1 citation statement)

References 10 publications

(8 reference statements)

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“…Brain RAS has already proven to have a role in the pathophysiology of depression [70]. As AT1 and AT2 receptors are found in the hypothalamus-pituitary-adrenal (HPA) [88] axis, HPA plays an important role in stress and stress-related behavior. Activation of corticotropin-releasing hormone (CRH) gene expression was found via AT1 receptor activation in immobilization-induced stress.…”

Section: History Of Brain Rasmentioning

confidence: 99%

Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It

Urmila

Patil

Nilam

et al. 2021

J Renin Angiotensin Aldosterone Syst

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The RAS (renin-angiotensin system) is the part of the endocrine system that plays a prime role in the control of essential hypertension. Since the discovery of brain RAS in the seventies, continuous efforts have been put by the scientific committee to explore it more. The brain has shown the presence of various components of brain RAS such as angiotensinogen (AGT), converting enzymes, angiotensin (Ang), and specific receptors (ATR). AGT acts as the precursor molecule for Ang peptides—I, II, III, and IV—while the enzymes such as prorenin, ACE, and aminopeptidases A and N synthesize it. AT1, AT2, AT4, and mitochondrial assembly receptor (MasR) are found to be plentiful in the brain. The brain RAS system exhibits pleiotropic properties such as neuroprotection and cognition along with regulation of blood pressure, CVS homeostasis, thirst and salt appetite, stress, depression, alcohol addiction, and pain modulation. The molecules acting through RAS predominantly ARBs and ACEI are found to be effective in various ongoing and completed clinical trials related to cognition, memory, Alzheimer’s disease (AD), and pain. The review summarizes the recent advances in the brain RAS system highlighting its significance in pathophysiology and treatment of the central nervous system-related disorders.

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Section: History Of Brain Rasmentioning

confidence: 99%

Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It

Urmila

Patil

Nilam

et al. 2021

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

show abstract

Investigation of poststroke epilepsy (INPOSE) study: a multicenter prospective study for prediction of poststroke epilepsy

et al. 2020

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Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury

Wei

Zhang

et al. 2016

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury (TBI) and the potential mechanisms related to the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier (BBB) integrity, the neurological function and histological injury were assessed, at the same time, the mRNA and protein expression levels of NLRP3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, NLRP3, apoptotic speck-containing protein (ASC) and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the NLRP3 inflammasome-regulated IL-1β and IL-18 accumulation.

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Evaluation and Comparison of Anticonvulsant Activity of t elmisartan and Olmesartan in Experimentally Induced Animal Models of Epilepsy

Cited by 6 publications

References 10 publications

Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It

Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It

Investigation of poststroke epilepsy (INPOSE) study: a multicenter prospective study for prediction of poststroke epilepsy

Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury

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