Sepsis-associated encephalopathy(SAE) is a brain dysfunction that occurs secondary to infection in the bo characterized by alteration of consciousness, ranging from delirium to coma, seizure or focal neurological sign...Sepsis-associated encephalopathy(SAE) is a brain dysfunction that occurs secondary to infection in the bo characterized by alteration of consciousness, ranging from delirium to coma, seizure or focal neurological signs. S involves a number of mechanisms, including neuroinflammation, in which the interaction between cytokines a acetylcholine results in neuronal loss and alterations in cholinergic signaling. Moreover, the interaction also occurs the periphery, accelerating a type of immunosuppressive state. Although its diagnosis is not specific in biochemis and imaging tests, it could potentiate severe outcomes, including increased mortality, cognitive decline, progress immunosuppression, cholinergic anti-inflammatory deficiency, and even metabolic and hydroelectrolyte imbalan Therefore, the bilateral communication between SAE and the multiple peripheral organs and especially the immu system should be emphasized in sepsis management.展开更多
Background:Excessive inflammatory responses play a critical role in the development of severe acute pancreatitis(SAP),and controlling such inflammation is vital for managing this often fatal disease.Dexmedetomidine ha...Background:Excessive inflammatory responses play a critical role in the development of severe acute pancreatitis(SAP),and controlling such inflammation is vital for managing this often fatal disease.Dexmedetomidine has been reported to possess protective properties in inflammatory diseases.Therefore,this study aimed to investigate whether dexmedetomidine pre-treatment exerts an anti-inflammatory effect in rats with SAP induced by sodium taurocholate,and if so,to determine the potential mechanism.Methods:SAP was induced with sodium taurocholate.Rats received an intraperitoneal injection of dexmedetomidine 30 min before sodium taurocholate administration.α-bungarotoxin,a selective alpha-7 nicotinic acetylcholine receptor(α7nAchR)antagonist,was injected intra-peritoneally 30 min before dexmedetomidine administration.The role of the vagus nerve was evaluated by performing unilateral cervical vagotomy before the administration of dexmedetomidine.Efferent discharge of the vagal nerve was recorded by the BL-420F Data Acquisition&Analysis System.Six hours after onset,serum pro-inflammatory cytokine(tumor necrosis factorα[TNF-α]and interleukin 6[IL-6])levels and amylase levels were determined using an enzyme-linked immunosorbent assay and an automated biochemical analyzer,respectively.Histopathological changes in the pancreas were observed after hematoxylin and eosin staining and scored according to Schmidt criteria.Results:Pre-treatment with dexmedetomidine significantly decreased serum levels of TNF-α,IL-6,and amylase,strongly alleviating pathological pancreatic injury in the rat model of SAP(TNF-α:174.2±30.2 vs.256.1±42.4 pg/ml;IL-6:293.3±46.8 vs.421.7±48.3 pg/ml;amylase:2102.3±165.3 vs.3186.4±245.2 U/L).However,the anti-inflammatory and pancreatic protective effects were abolished after vagotomy or pre-administration ofα-bungarotoxin.Dexmedetomidine also significantly increased the discharge frequency and amplitude of the cervical vagus nerve in the SAP rat model(discharge frequency:456.8±50.3 vs.332.4±展开更多
非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清...非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清窍失养,发为痴呆。胆碱能通路与认知障碍的发生发展密切相关,包括神经递质乙酰胆碱的缺乏、脑白质病变影响胆碱能通路的网络连接以及胆碱能抗炎通路等。探讨中医虚痰瘀的病机演变与胆碱能通路发病机制之间的关系,有助于进一步发掘中医中药治疗在胆碱能通路的作用。展开更多
Acetylcholine(ACh)regulates inflammation viaα7 nicotinic acetylcholine receptor(α7 nAChR).Acetylcholinesterase(AChE),an enzyme hydrolyzing ACh,is expressed in immune cells suggesting non-classical function in inflam...Acetylcholine(ACh)regulates inflammation viaα7 nicotinic acetylcholine receptor(α7 nAChR).Acetylcholinesterase(AChE),an enzyme hydrolyzing ACh,is expressed in immune cells suggesting non-classical function in inflammatory responses.Here,the expression of PRiMA-linked G4 AChE was identified on the surface of macrophages.In lipopolysaccharide-induced inflammatory processes,AChE was upregulated by the binding of NF-κB onto the ACHE promotor.Conversely,the overexpression of G4 AChE inhibited ACh-suppressed cytokine release and cell migration,which was in contrast to that of applied AChE inhibitors.AChEmt,a DNA construct without enzymatic activity,was adopted to identify the protein role of AChE in immune system.Overexpression of G4 AChEmt induced cell migration and inhibited ACh-suppressed cell migration.The co-localization ofα7 nAChR and AChE was found in macrophases,suggesting the potential interaction ofα7 nAChR and AChE.Besides,immunoprecipitation showed a close association ofα7 nAChR and AChE protein in cell membrane.Hence,the novel function of AChE in macrophage by interacting withα7 nAChR was determined.Together with hydrolysis of ACh,AChE plays a direct role in the regulation of inflammatory response.As such,AChE could serve as a novel target to treat age-related diseases by antiinflammatory responses.展开更多
Sepsis is a life-threatening inflammatory syndrome with high morbidity and mortality rates.However,options for sepsis are still limited to general treatment in intensive care units(ICUs),and effective therapies that i...Sepsis is a life-threatening inflammatory syndrome with high morbidity and mortality rates.However,options for sepsis are still limited to general treatment in intensive care units(ICUs),and effective therapies that improve sepsis survival are required.Immune disturbances play a vital role in the pathology of sepsis and are associated with protracted inflammation,susceptibility to infections,and death.Therefore,many investigators have focused on the potential benefits of immunomodulation therapy for sepsis.Electroacupuncture(EA)has been practiced in clinics for many years and has shown advantages in treating infectious diseases.Over the last few decades,our understanding of the efficacy and mechanisms of EA in sepsis has undergone considerable developments.We searched the literature regarding“CNKI,Wan Fang Data,VIP Database,PubMed,and Ingenta Connect”from 2010 to 2023,using the keywords“sepsis”“septic”and“electroacupuncture”and 336 sources were searched.Finally,we included 82 studies that targeted the immune system to determine EA’s anti-inflammatory and immunomodulatory effects on sepsis.In this review,we found that EA has clinical benefits in relieving septic inflammation,improving immune function,and attenuating related multi-organ injury through several mechanisms,such as activation of the cholinergic anti-inflammatory pathway(CAP),vagaladrenal axis,inhibition of the nuclear factor Kappa-B(NF-κB)signaling pathway,signal transducers and activators of transcription(STAT)signaling pathway,and improvement of immune cell function.Therefore,EA may be a promising complementary therapy for sepsis treatment.We also expect these data will contribute to further studies on EA in sepsis.展开更多
Pre-eclampsia is characterized by an excessive maternal inflammatory response.The cholinergic antiinflammatory pathway(CAP)has been shown as the efferent arm of a vagal reflex with the potential to limit inflammatory ...Pre-eclampsia is characterized by an excessive maternal inflammatory response.The cholinergic antiinflammatory pathway(CAP)has been shown as the efferent arm of a vagal reflex with the potential to limit inflammatory responses.Therefore,in this study,the CAP regulation through the nervous vagal stimulation(VNS)reduced the severity of NG-nitro-L-arginine methyl ester(L-NAME)-induced pre-eclampsia was determined in a rat model.Rats were given 125 mg/kg/day of L-NAME via subcutaneous injection on gestational day(GD)10–16.In addition,the rats were treated by active or sham electrical stimulation once a day during GD 13–19.Systolic blood pressure(SBP),urinary albumin,and pregnancy outcomes were documented for each rat.The average fetal weights and crown-rump length(CRL)as well as the placental weights of rats in both control and experimental groups were recorded onthe 13th day,16th day and 20th day of gestation.Subsequently,placentas were collected from the rats on GD20 to measure the level of cytokines.In addition,qRT-PCR and Western blot analysis were used to detect the mRNA and protein expression ofα7 nicotinic acetylcholine receptor(α7nAChR)and nuclear factor-κB(NF-κB),respectively.Immunohistochemistry assays were also carried out to determine the location and level ofα7nAChR and NF-κB in placentas.CAP regulation through the transcutaneous auricular nerve stimulation alleviated the clinical symptoms in the rats after L-NAME induction,including hypertension,proteinuria,fetal growth retardation and fetal death.In addition,TaVNS also increasedα7nAChR expression,reduced NF-κB p65 expression,and reversed LNAME-induced proinflammatory cytokines in the placenta tissues,including tumor necrosis factor-alpha(TNF-α),high mobility group box 1(HMGB-1)and interleukin-6(IL-6).The findings of this study showed that TaVNS might be used as a promising tool to attenuate pre-eclampsia-like symptoms.In addition,the protective effect of TaVNS was associated with the improvement ofα7nAChR expression and the inhibition of 展开更多
The cholinergic anti-inflammatory pathway(CAP)refers to the anti-inflammatory effects mediated by the parasympathetic nervous system.Existence of this pathway was first demonstrated when acetylcholinesterase inhibitor...The cholinergic anti-inflammatory pathway(CAP)refers to the anti-inflammatory effects mediated by the parasympathetic nervous system.Existence of this pathway was first demonstrated when acetylcholinesterase inhibitors showed benefits in animal models of sepsis.CAP functions via the vagus nerve.The systemic antiinflammatory effects of CAP converges on theα7 nicotinic acetylcholine receptor on splenic macrophages,leading to suppression of pro-inflammatory cytokines and simultaneous stimulation of anti-inflammatory cytokines,including interleukin 10.CAP offers a novel mechanism to mitigate inflammation.Electrical vagal nerve stimulation has shown benefits in patients suffering from rheumatoid arthritis.Direct agonists like nicotine and GTS-1 have also demonstrated antiinflammatory properties in models of sepsis and acute respiratory distress syndrome,as have acetylcholinesterase inhibitors like Galantamine and Physostigmine.Experience with coronavirus disease 2019(COVID-19)induced acute respiratory distress syndrome indicates that immunomodulators have a protective role in patient outcomes.Dexamethasone is the only medication currently in use that has shown to improve clinical outcomes.This is likely due to the suppression of what is referred to as a cytokine storm,which is implicated in the lethality of viral pneumonia.Nicotine transdermal patch activates CAP and harvests its anti-inflammatory potential by means of an easily administered depot delivery mechanism.It could prove to be a promising,safe and inexpensive additional tool in the currently limited armamentarium at our disposal for management of COVID-19 induced acute hypoxic respiratory failure.展开更多
Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats....Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats. Recent findings regarding stroke pathophysiology have recognized that anti-inflammation is an important target for the treatment of ischemic stroke. The cholinergic anti-inflammatory pathway is a highly robust neural-immune mechanism for inflammation control. This study was to investigate whether activating the cholinergic anti-inflammatory pathway can be involved in the mechanism of inhibiting the inflammatory response during puerarin-induced cerebral ischemia/reperfusion in rats. Results showed that puerarin pretreatment （intravenous injection） re- duced the ischemic infarct volume, improved neurological deficit after cerebral ischemia/reperfusion and decreased the levels of interleukin-1β, interleukin-6 and tumor necrosis factor-a in brain tissue. Pretreatment with puerarin （intravenous injection） attenuated the inflammatory response in rats, which was accompanied by janus-activated kinase 2 （JAK2） and signal transducers and activators of transcription 3 （STAT3） activation and nuclear factor kappa B （NF-KB） inhibition. These observa- tions were inhibited by the alpha7 nicotinic acetylcholine receptor （a7nAchR） antagonist a-bungarotoxin （a-BGT）. In addition, puerarin pretreatment increased the expression of a7nAchR mRNA in ischemic cerebral tissue. These data demonstrate that puerarin pretreatment strongly protects the brain against cerebral ischemia/reperfusion injury and inhibits the inflammatory re- sponse. Our results also indicated that the anti-inflammatory effect of puerarin may partly be medi- ated through the activation of the cholinergic anti-inflammatory pathway.展开更多
基金supported by National Natural Science Foundation of China (81272089, 81130035, 81372054, and 81121004)the National Basic Research Program of China (2012CB518102)the "Twelve-Five Plan" for Military Scientific Foundation (BWS12J050)
文摘Sepsis-associated encephalopathy(SAE) is a brain dysfunction that occurs secondary to infection in the bo characterized by alteration of consciousness, ranging from delirium to coma, seizure or focal neurological signs. S involves a number of mechanisms, including neuroinflammation, in which the interaction between cytokines a acetylcholine results in neuronal loss and alterations in cholinergic signaling. Moreover, the interaction also occurs the periphery, accelerating a type of immunosuppressive state. Although its diagnosis is not specific in biochemis and imaging tests, it could potentiate severe outcomes, including increased mortality, cognitive decline, progress immunosuppression, cholinergic anti-inflammatory deficiency, and even metabolic and hydroelectrolyte imbalan Therefore, the bilateral communication between SAE and the multiple peripheral organs and especially the immu system should be emphasized in sepsis management.
基金This work was supported by a grant from the National Natural Sciences Foundation of China(No.81672449)。
文摘Background:Excessive inflammatory responses play a critical role in the development of severe acute pancreatitis(SAP),and controlling such inflammation is vital for managing this often fatal disease.Dexmedetomidine has been reported to possess protective properties in inflammatory diseases.Therefore,this study aimed to investigate whether dexmedetomidine pre-treatment exerts an anti-inflammatory effect in rats with SAP induced by sodium taurocholate,and if so,to determine the potential mechanism.Methods:SAP was induced with sodium taurocholate.Rats received an intraperitoneal injection of dexmedetomidine 30 min before sodium taurocholate administration.α-bungarotoxin,a selective alpha-7 nicotinic acetylcholine receptor(α7nAchR)antagonist,was injected intra-peritoneally 30 min before dexmedetomidine administration.The role of the vagus nerve was evaluated by performing unilateral cervical vagotomy before the administration of dexmedetomidine.Efferent discharge of the vagal nerve was recorded by the BL-420F Data Acquisition&Analysis System.Six hours after onset,serum pro-inflammatory cytokine(tumor necrosis factorα[TNF-α]and interleukin 6[IL-6])levels and amylase levels were determined using an enzyme-linked immunosorbent assay and an automated biochemical analyzer,respectively.Histopathological changes in the pancreas were observed after hematoxylin and eosin staining and scored according to Schmidt criteria.Results:Pre-treatment with dexmedetomidine significantly decreased serum levels of TNF-α,IL-6,and amylase,strongly alleviating pathological pancreatic injury in the rat model of SAP(TNF-α:174.2±30.2 vs.256.1±42.4 pg/ml;IL-6:293.3±46.8 vs.421.7±48.3 pg/ml;amylase:2102.3±165.3 vs.3186.4±245.2 U/L).However,the anti-inflammatory and pancreatic protective effects were abolished after vagotomy or pre-administration ofα-bungarotoxin.Dexmedetomidine also significantly increased the discharge frequency and amplitude of the cervical vagus nerve in the SAP rat model(discharge frequency:456.8±50.3 vs.332.4±
文摘非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清窍失养,发为痴呆。胆碱能通路与认知障碍的发生发展密切相关,包括神经递质乙酰胆碱的缺乏、脑白质病变影响胆碱能通路的网络连接以及胆碱能抗炎通路等。探讨中医虚痰瘀的病机演变与胆碱能通路发病机制之间的关系,有助于进一步发掘中医中药治疗在胆碱能通路的作用。
基金supported by Shenzhen Science and Technology Committee Research Grant(JCYJ20170413173747440,ZDSYS 201707281432317,JCYJ20180306174903174,CKFW2016082916015476,China)China Post-doctoral Science Foundation(2019M653087)+3 种基金Zhongshan Municipal Bureau of Science and Technology(ZSST20SC03,China)Guangzhou Science and Technology Committee Research Grant(GZSTI16SC02 and GZSTI17SC02,China)Hong Kong RGC Theme-based Research Scheme(T13-607/12R,China)Hong Kong Innovation Technology Fund(UIM/340,UIM/385,ITS/500/18FP,TCPD/17e9,PD18SC01 and HMRF18SC06,China)
文摘Acetylcholine(ACh)regulates inflammation viaα7 nicotinic acetylcholine receptor(α7 nAChR).Acetylcholinesterase(AChE),an enzyme hydrolyzing ACh,is expressed in immune cells suggesting non-classical function in inflammatory responses.Here,the expression of PRiMA-linked G4 AChE was identified on the surface of macrophages.In lipopolysaccharide-induced inflammatory processes,AChE was upregulated by the binding of NF-κB onto the ACHE promotor.Conversely,the overexpression of G4 AChE inhibited ACh-suppressed cytokine release and cell migration,which was in contrast to that of applied AChE inhibitors.AChEmt,a DNA construct without enzymatic activity,was adopted to identify the protein role of AChE in immune system.Overexpression of G4 AChEmt induced cell migration and inhibited ACh-suppressed cell migration.The co-localization ofα7 nAChR and AChE was found in macrophases,suggesting the potential interaction ofα7 nAChR and AChE.Besides,immunoprecipitation showed a close association ofα7 nAChR and AChE protein in cell membrane.Hence,the novel function of AChE in macrophage by interacting withα7 nAChR was determined.Together with hydrolysis of ACh,AChE plays a direct role in the regulation of inflammatory response.As such,AChE could serve as a novel target to treat age-related diseases by antiinflammatory responses.
基金funded by the National Key Research and Development Program(2022YFC3500704)the National Natural Science Foundation of China(82174500,82004491).
文摘Sepsis is a life-threatening inflammatory syndrome with high morbidity and mortality rates.However,options for sepsis are still limited to general treatment in intensive care units(ICUs),and effective therapies that improve sepsis survival are required.Immune disturbances play a vital role in the pathology of sepsis and are associated with protracted inflammation,susceptibility to infections,and death.Therefore,many investigators have focused on the potential benefits of immunomodulation therapy for sepsis.Electroacupuncture(EA)has been practiced in clinics for many years and has shown advantages in treating infectious diseases.Over the last few decades,our understanding of the efficacy and mechanisms of EA in sepsis has undergone considerable developments.We searched the literature regarding“CNKI,Wan Fang Data,VIP Database,PubMed,and Ingenta Connect”from 2010 to 2023,using the keywords“sepsis”“septic”and“electroacupuncture”and 336 sources were searched.Finally,we included 82 studies that targeted the immune system to determine EA’s anti-inflammatory and immunomodulatory effects on sepsis.In this review,we found that EA has clinical benefits in relieving septic inflammation,improving immune function,and attenuating related multi-organ injury through several mechanisms,such as activation of the cholinergic anti-inflammatory pathway(CAP),vagaladrenal axis,inhibition of the nuclear factor Kappa-B(NF-κB)signaling pathway,signal transducers and activators of transcription(STAT)signaling pathway,and improvement of immune cell function.Therefore,EA may be a promising complementary therapy for sepsis treatment.We also expect these data will contribute to further studies on EA in sepsis.
基金Provincial Natural Science Foundation of China Hainan(819MS119).
文摘Pre-eclampsia is characterized by an excessive maternal inflammatory response.The cholinergic antiinflammatory pathway(CAP)has been shown as the efferent arm of a vagal reflex with the potential to limit inflammatory responses.Therefore,in this study,the CAP regulation through the nervous vagal stimulation(VNS)reduced the severity of NG-nitro-L-arginine methyl ester(L-NAME)-induced pre-eclampsia was determined in a rat model.Rats were given 125 mg/kg/day of L-NAME via subcutaneous injection on gestational day(GD)10–16.In addition,the rats were treated by active or sham electrical stimulation once a day during GD 13–19.Systolic blood pressure(SBP),urinary albumin,and pregnancy outcomes were documented for each rat.The average fetal weights and crown-rump length(CRL)as well as the placental weights of rats in both control and experimental groups were recorded onthe 13th day,16th day and 20th day of gestation.Subsequently,placentas were collected from the rats on GD20 to measure the level of cytokines.In addition,qRT-PCR and Western blot analysis were used to detect the mRNA and protein expression ofα7 nicotinic acetylcholine receptor(α7nAChR)and nuclear factor-κB(NF-κB),respectively.Immunohistochemistry assays were also carried out to determine the location and level ofα7nAChR and NF-κB in placentas.CAP regulation through the transcutaneous auricular nerve stimulation alleviated the clinical symptoms in the rats after L-NAME induction,including hypertension,proteinuria,fetal growth retardation and fetal death.In addition,TaVNS also increasedα7nAChR expression,reduced NF-κB p65 expression,and reversed LNAME-induced proinflammatory cytokines in the placenta tissues,including tumor necrosis factor-alpha(TNF-α),high mobility group box 1(HMGB-1)and interleukin-6(IL-6).The findings of this study showed that TaVNS might be used as a promising tool to attenuate pre-eclampsia-like symptoms.In addition,the protective effect of TaVNS was associated with the improvement ofα7nAChR expression and the inhibition of
文摘The cholinergic anti-inflammatory pathway(CAP)refers to the anti-inflammatory effects mediated by the parasympathetic nervous system.Existence of this pathway was first demonstrated when acetylcholinesterase inhibitors showed benefits in animal models of sepsis.CAP functions via the vagus nerve.The systemic antiinflammatory effects of CAP converges on theα7 nicotinic acetylcholine receptor on splenic macrophages,leading to suppression of pro-inflammatory cytokines and simultaneous stimulation of anti-inflammatory cytokines,including interleukin 10.CAP offers a novel mechanism to mitigate inflammation.Electrical vagal nerve stimulation has shown benefits in patients suffering from rheumatoid arthritis.Direct agonists like nicotine and GTS-1 have also demonstrated antiinflammatory properties in models of sepsis and acute respiratory distress syndrome,as have acetylcholinesterase inhibitors like Galantamine and Physostigmine.Experience with coronavirus disease 2019(COVID-19)induced acute respiratory distress syndrome indicates that immunomodulators have a protective role in patient outcomes.Dexamethasone is the only medication currently in use that has shown to improve clinical outcomes.This is likely due to the suppression of what is referred to as a cytokine storm,which is implicated in the lethality of viral pneumonia.Nicotine transdermal patch activates CAP and harvests its anti-inflammatory potential by means of an easily administered depot delivery mechanism.It could prove to be a promising,safe and inexpensive additional tool in the currently limited armamentarium at our disposal for management of COVID-19 induced acute hypoxic respiratory failure.
基金supported by the Young Scientists Foundation of Hubei Provincial Health Department,No.QJX2012-16
文摘Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats. Recent findings regarding stroke pathophysiology have recognized that anti-inflammation is an important target for the treatment of ischemic stroke. The cholinergic anti-inflammatory pathway is a highly robust neural-immune mechanism for inflammation control. This study was to investigate whether activating the cholinergic anti-inflammatory pathway can be involved in the mechanism of inhibiting the inflammatory response during puerarin-induced cerebral ischemia/reperfusion in rats. Results showed that puerarin pretreatment （intravenous injection） re- duced the ischemic infarct volume, improved neurological deficit after cerebral ischemia/reperfusion and decreased the levels of interleukin-1β, interleukin-6 and tumor necrosis factor-a in brain tissue. Pretreatment with puerarin （intravenous injection） attenuated the inflammatory response in rats, which was accompanied by janus-activated kinase 2 （JAK2） and signal transducers and activators of transcription 3 （STAT3） activation and nuclear factor kappa B （NF-KB） inhibition. These observa- tions were inhibited by the alpha7 nicotinic acetylcholine receptor （a7nAchR） antagonist a-bungarotoxin （a-BGT）. In addition, puerarin pretreatment increased the expression of a7nAchR mRNA in ischemic cerebral tissue. These data demonstrate that puerarin pretreatment strongly protects the brain against cerebral ischemia/reperfusion injury and inhibits the inflammatory re- sponse. Our results also indicated that the anti-inflammatory effect of puerarin may partly be medi- ated through the activation of the cholinergic anti-inflammatory pathway.
