Nodakenin alleviates renal ischaemia‐reperfusion injury via inhibiting reactive oxygen species‐induced NLRP3 inflammasome activation

Nephrology ◽  
2020 ◽  
Vol 26 (1) ◽  
pp. 78-87
Author(s):  
Yuan Liao ◽  
Xiao Lin ◽  
Jianchun Li ◽  
Ruizhi Tan ◽  
Xia Zhong ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Nlrp3 Inflammasome ◽  
Reactive Oxygen ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Nlrp3 Inflammasome Activation

scholarly journals Naoxintong attenuates Ischaemia/reperfusion Injury through inhibiting NLRP3 inflammasome activation

2016 ◽  
Vol 21 (1) ◽  
pp. 4-12 ◽  
Author(s):  
Yaqiong Wang ◽  
Xiaoxiang Yan ◽  
Shouling Mi ◽  
Zhang Li ◽  
Yuexiang Wang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Nlrp3 Inflammasome Activation

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

2016 ◽  
Vol 130 (18) ◽  
pp. 1641-1653 ◽  
Author(s):  
Yuanna Ling ◽  
Guiming Chen ◽  
Yi Deng ◽  
Huixiong Tang ◽  
Long Ling ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Reactive Oxygen ◽  
Post Treatment ◽  
Autophagic Flux ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

The present paper provides evidence that polydatin (PD) post-treatment alleviates myocardial ischaemia/reperfusion (I/R) injury by promoting autophagic flux to clear damaged mitochondria to reduce reactive oxygen species (ROS) and cell death.

scholarly journals Icarisid I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity

2020 ◽  
Author(s):  
Yuan Gao ◽  
Guang Xu ◽  
Li Ma ◽  
Wei Shi ◽  
Zhilei Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Nlrp3 Inflammasome ◽  
Bone Fractures ◽  
Reactive Oxygen ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Hepatocyte Apoptosis ◽  
Specific Stimulus ◽  
Nlrp3 Inflammasome Activation

Abstract Background Epimedii Folium(EF) is commonly used for treating bone fractures and joint diseases, but the potential hepatotoxicity of EF limits its clinical application. Our previous study confirms that EF could lead to idiosyncratic drug-induced liver injury (IDILI) and hepatocyte apoptosis, but the mechanism remains unknown. Studies have shown that NLRP3 inflammasome plays an important role in the development of various inflammatory diseases such as IDILI. Specific stimulus-induced NLRP3 inflammasome activation may has been a key strategy for lead to liver injury. Therefore, main compounds derived from EF were chosen to test whether the ingredients in EF could activate the NLRP3 inflammasome and to induce IDILI. Methods Mouse were treated with Icariside I, and then stimulated with inflammasome stimuli and assayed for the production of caspase-1 and interleukin 1β (IL-1β) and the release of lactate dehydrogenase (LDH). Determination of intracellular potassium, ASC oligomerization as well as reactive oxygen species (ROS) production were used to evaluate the stimulative mechanism of Icariside I on inflammasome activation. Mouse models of NLRP3 diseases were used to test whether Icariside I has hepatocyte apoptosis effects and promoted NLRP3 inflammasome activation in vivo. Results Icariside I specifically enhances NLRP3 inflammasome activation triggered by ATP or nigericin but not SiO2, poly(I:C) or cytosolic LPS. Additionally, Icariside I does not alter the activation of NLRC4 and AIM2 inflammasomes. Mechanically, Icariside I alone does not induce mitochondrial reactive oxygen species (mtROS), which is one of the critical upstream events of NLRP3 inflammasome activation; however, Icariside I increases mtROS production induced by ATP or nigericin but not SiO2. Importantly, Icariside I leads to liver injury and NLRP3 inflammasome activation in an LPS-mediated susceptibility mouse model of IDILI, but the effect of Icariside I is absent in the LPS-mediated mice model pretreated with MCC950, which is used to mimic knockdown of NLRP3 inflammasome activation. Conclusions Our study reveals that Icariside I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. The findings suggest that Icariside I or EF should be avoided in patients with diseases related to ATP or nigericin-induced NLRP3 inflammasome activation, which may be risk factors for IDILI.

scholarly journals Icariside I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity

2020 ◽  
Author(s):  
Yuan Gao ◽  
Zhaofang Bai ◽  
Xiaohe Xiao ◽  
guang Xu ◽  
ming Niu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Nlrp3 Inflammasome ◽  
Bone Fractures ◽  
Reactive Oxygen ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Hepatocyte Apoptosis ◽  
Specific Stimulus ◽  
Nlrp3 Inflammasome Activation

Abstract Background: Epimedii Folium(EF) is commonly used for treating bone fractures and joint diseases, but the potential hepatotoxicity of EF limits its clinical application. Our previous study confirms that EF could lead to idiosyncratic drug-induced liver injury (IDILI) and hepatocyte apoptosis, but the mechanism remains unknown. Studies have shown that NLRP3 inflammasome plays an important role in the development of various inflammatory diseases such as IDILI. Specific stimulus-induced NLRP3 inflammasome activation may has been a key strategy for lead to liver injury. Therefore, main compounds derived from EF were chosen to test whether the ingredients in EF could activate the NLRP3 inflammasome and to induce IDILI.Methods: Mouse were treated with Icariside I, and then stimulated with inflammasome stimuli and assayed for the production of caspase-1 and interleukin 1β (IL-1β) and the release of lactate dehydrogenase (LDH). Determination of intracellular potassium, ASC oligomerization as well as reactive oxygen species (ROS) production were used to evaluate the stimulative mechanism of Icariside I on inflammasome activation. Mouse models of NLRP3 diseases were used to test whether Icariside I has hepatocyte apoptosis effects and promoted NLRP3 inflammasome activation in vivo.Results: Icariside I specifically enhances NLRP3 inflammasome activation triggered by ATP or nigericin but not SiO2, poly(I:C) or cytosolic LPS. Additionally, Icariside I does not alter the activation of NLRC4 and AIM2 inflammasomes. Mechanically, Icariside I alone does not induce mitochondrial reactive oxygen species (mtROS), which is one of the critical upstream events of NLRP3 inflammasome activation; however, Icariside I increases mtROS production induced by ATP or nigericin but not SiO2. Importantly, Icariside I leads to liver injury and NLRP3 inflammasome activation in an LPS-mediated susceptibility mouse model of IDILI, but the effect of Icariside I is absent in the LPS-mediated mice model pretreated with MCC950, which is used to mimic knockdown of NLRP3 inflammasome activation.Conclusions: Our study reveals that Icariside I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. The findings suggest that Icariside I or EF should be avoided in patients with diseases related to ATP or nigericin-induced NLRP3 inflammasome activation, which may be risk factors for IDILI.

scholarly journals MCP-1 induces cardioprotection against ischaemia/reperfusion injury: role of reactive oxygen species

2008 ◽  
Vol 78 (3) ◽  
pp. 554-562 ◽  
Author(s):  
Hajime Morimoto ◽  
Masamichi Hirose ◽  
Masafumi Takahashi ◽  
Masanori Kawaguchi ◽  
Hirohiko Ise ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals Icarisid I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity

2019 ◽  
Author(s):  
Yuan Gao ◽  
Zhaofang Bai ◽  
Xiaohe Xiao ◽  
Guang Xu ◽  
Ming Niu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Nlrp3 Inflammasome ◽  
Bone Fractures ◽  
Reactive Oxygen ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Hepatocyte Apoptosis ◽  
Specific Stimulus ◽  
Nlrp3 Inflammasome Activation

Abstract Background Epimedii Folium(EF) is commonly used for treating bone fractures and joint diseases, but the potential hepatotoxicity of EF limits its clinical application. Our previous study confirms that EF could lead to idiosyncratic drug-induced liver injury (IDILI) and hepatocyte apoptosis, but the mechanism remains unknown. Studies have shown that NLRP3 inflammasome plays an important role in the development of various inflammatory diseases such as IDILI. Specific stimulus-induced NLRP3 inflammasome activation may has been a key strategy for lead to liver injury. Therefore, main compounds derived from EF were chosen to test whether the ingredients in EF could activate the NLRP3 inflammasome and to induce IDILI.Methods Mouse were treated with Icarisid I, and then stimulated with inflammasome stimuli and assayed for the production of caspase-1 and interleukin 1β (IL-1β) and the release of lactate dehydrogenase (LDH). Determination of intracellular potassium, ASC oligomerization as well as reactive oxygen species (ROS) production were used to evaluate the stimulative mechanism of Icarisid I on inflammasome activation. Mouse models of NLRP3 diseases were used to test whether Icarisid I has hepatocyte apoptosis effects and promoted NLRP3 inflammasome activation in vivo.Results Icarisid I specifically enhances NLRP3 inflammasome activation triggered by ATP or nigericin but not SiO2, poly(I:C) or cytosolic LPS. Additionally, Icarisid I does not alter the activation of NLRC4 and AIM2 inflammasomes. Mechanically, Icarisid I alone does not induce mitochondrial reactive oxygen species (mtROS), which is one of the critical upstream events of NLRP3 inflammasome activation; however, Icarisid I increases mtROS production induced by ATP or nigericin but not SiO2. Importantly, Icarisid I leads to liver injury and NLRP3 inflammasome activation in an LPS-mediated susceptibility mouse model of IDILI, but the effect of Icarisid I is absent in the LPS-mediated mice model pretreated with MCC950, which is used to mimic knockdown of NLRP3 inflammasome activation.Conclusions Our study reveals that Icarisid I specifically facilitates ATP or nigericin-induced NLRP3 inflammasome activation and causes idiosyncratic hepatotoxicity. The findings suggest that Icarisid I or EF should be avoided in patients with diseases related to ATP or nigericin-induced NLRP3 inflammasome activation, which may be risk factors for IDILI.

Sign in / Sign up

Export Citation Format

Share Document