“…Shen et al reported that CY-09 inhibited the NLRP3 driven neuroinflammation in a PTZ-induced kindling mouse model, a chronic model of generalized seizures [144]. CY-09 repressed the expression of NLRP3, IL-1 and IL-18 in injured brain tissue in the rat TBI models [145]. The findings from Wang et al showed that CY-09 attenuates depression-like behaviors by inhibiting the NLRP3-mediated neuroinflammation in LPS-induced mice [146].…”
Epilepsy is one of the most prevalent and serious brain disorders, affecting 70 million people worldwide. Antiseizure medications (ASMs) though relieve symptoms and prevent the occurrence of future seizures in epileptic patients have limited effect on epileptogenesis. Addressing the multifaceted nature of epileptogenesis and its association with Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated neuroinflammation requires a comprehensive understanding of the underlying mechanisms for development of targeted therapeutic strategies beyond conventional antiseizure treatments. Several types of NLRP3 inhibitors have been developed and their effect has been validated both in vitro and in vivo models of epileptogenesis. In this review, we discuss the advances in understanding the regulatory mechanisms of NLRP3 activation as well as progress made and challenges facing in the development of NLRP3 inhibitors for the treatment of epilepsy.
“…Shen et al reported that CY-09 inhibited the NLRP3 driven neuroinflammation in a PTZ-induced kindling mouse model, a chronic model of generalized seizures [144]. CY-09 repressed the expression of NLRP3, IL-1 and IL-18 in injured brain tissue in the rat TBI models [145]. The findings from Wang et al showed that CY-09 attenuates depression-like behaviors by inhibiting the NLRP3-mediated neuroinflammation in LPS-induced mice [146].…”
Epilepsy is one of the most prevalent and serious brain disorders, affecting 70 million people worldwide. Antiseizure medications (ASMs) though relieve symptoms and prevent the occurrence of future seizures in epileptic patients have limited effect on epileptogenesis. Addressing the multifaceted nature of epileptogenesis and its association with Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated neuroinflammation requires a comprehensive understanding of the underlying mechanisms for development of targeted therapeutic strategies beyond conventional antiseizure treatments. Several types of NLRP3 inhibitors have been developed and their effect has been validated both in vitro and in vivo models of epileptogenesis. In this review, we discuss the advances in understanding the regulatory mechanisms of NLRP3 activation as well as progress made and challenges facing in the development of NLRP3 inhibitors for the treatment of epilepsy.
“…Shen et al reported that CY-09 inhibited the NLRP3 driven neuroinflammation in PTZ induced kindling mouse model, a chronic model of generalized seizures [146]. CY-09 repressed the expression of NLRP3, IL-1b and IL-18 in injured brain tissue in the rat TBI models [147]. The findings from Wang et al showed that CY-09 attenuates depression-like behaviors by inhibiting the NLRP3-mediated neuroinflammation in LPS-induced mice [148].…”
Section: Nlrp3 Inhibitors In Preclinical and Clinical Trial Phasementioning
Epilepsy is one of the most prevalent and serious brain disorders, affecting 70 million people worldwide. Antiseizure medications (ASMs) though relieve symptoms and prevent the occurrence of future seizures in epileptic patients have limited effect on epileptogenesis. Addressing the multifaceted nature of epileptogenesis and its association with Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated neuroinflammation requires a comprehensive understanding of the underlying mechanisms for development of targeted therapeutic strategies beyond conventional antiseizure treatments. Several types of NLRP3 inhibitors have been developed and their effect has been validated both in vitro and in vivo models of epileptogenesis. In this review, we discuss the advances in understanding the regulatory mechanisms of NLRP3 activation as well as progress made and challenges facing in the development of NLRP3 inhibitors for the treatment of epilepsy.
“…Shen et al reported that CY-09 inhibited the NLRP3 driven neuroinflammation in a PTZ-induced kindling mouse model, a chronic model of generalized seizures [ 144 ]. CY-09 repressed the expression of NLRP3, IL-1β, and IL-18 in injured brain tissue in the rat TBI models [ 145 ]. The findings from Wang et al showed that CY-09 attenuates depression-like behaviors by inhibiting the NLRP3-mediated neuroinflammation in LPS-induced mice [ 146 ].…”
Epilepsy is one of the most prevalent and serious brain disorders and affects over 70 million people globally. Antiseizure medications (ASMs) relieve symptoms and prevent the occurrence of future seizures in epileptic patients but have a limited effect on epileptogenesis. Addressing the multifaceted nature of epileptogenesis and its association with the Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated neuroinflammation requires a comprehensive understanding of the underlying mechanisms of these medications for the development of targeted therapeutic strategies beyond conventional antiseizure treatments. Several types of NLRP3 inhibitors have been developed and their effect has been validated both in in vitro and in vivo models of epileptogenesis. In this review, we discuss the advances in understanding the regulatory mechanisms of NLRP3 activation as well as progress made, and challenges faced in the development of NLRP3 inhibitors for the treatment of epilepsy.
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