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
Objective： Acupuncture has a definite therapeutic effect on chronic obstructive pulmonary disease （COPD）, and the cholinergic anti-inflammatory pathway （CAP） has been shown to be involved in regula- tion of infla...Objective： Acupuncture has a definite therapeutic effect on chronic obstructive pulmonary disease （COPD）, and the cholinergic anti-inflammatory pathway （CAP） has been shown to be involved in regula- tion of inflammation. In this study, we investigated whether electro-acupuncture （EA） affects the CAP in COPD,Methods： Sprague-Dawley rats were induced into COPD through exposure to cigarette smoke combined with lipopolysaccharide. EA treatment was applied at Zusanli （ST36） and Feishu （BL13） points for 30 min/d for 7 d. Seventy-two rats were randomly divided into six study groups, including normal, normal ＋ EA, normal ＋ α-bungarotoxin （α-BGT） （the antagonist of the nicotinic acetylcholine receptor α7 subunit （α7nAChR）） ＋ EA, COPD, COPD ＋ EA, and COPD ＋ α-BGT ＋ EA. Lung function, pathology and vagus nerve discharge were tested. The levels of acetylcholine （ACh）, acetylcholinesterase （ACHE）, interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-ct） in bronchoalveolar lavage fluid （BALF） and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreac- tivity of α7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 （JAK2）, sig- nal transducers and activators of transcription 3 （STAT3）, nuclear factor-KB （NF-KB）, were observed by quantitative reverse transcription-polymerase chain reaction, Western blot and immunohistochemistry. Results： Compared with normal rats, there were a significant decline in lung function and discharge of the vagus nerve （P 〈 0.01）, a marked sign of lung inflammation and an increase of ACh, ACHE, IL-6 and TNF-α level in BALF or lung tissue （P 〈 0.05, P 〈 0.01 ） and higher expression of 0t7nAChR, JAK2, STAT3 and NF-αB （P 〈 0.05, P 〈 0.01） in the COPD rats. In rats receiving EA, the lung function and vagal discharge were enhanced （P 〈 0.01 ）, lung inflammation was improved and the levels of ACh, ACHE, IL-展开更多
Background： Shensong Yangxin （SSYX）, a traditional Chinese herbal medicine, has long been used clinically to treat arrhythmias in China. However, the mechanism of SSYX on atrial fibrillation （AF） is unknown. In t...Background： Shensong Yangxin （SSYX）, a traditional Chinese herbal medicine, has long been used clinically to treat arrhythmias in China. However, the mechanism of SSYX on atrial fibrillation （AF） is unknown. In this study, we tested the hypothesis that the effect of SSYX on the progression of paroxysmal AF is correlated with the regulation of autonomic nerve activity. Methods： Eighteen mongrel dogs were randomly divided into control group （n = 6）, pacing group （n = 6）, and pacing ＋ SSYX group （n = 6）. The control group was implanted with pacemakers without pacing; the pacing group was implanted with pacemakers with long-term intermittent atrial pacing; the pacing ＋ SSYX group underwent long-term intermittent atrial pacing and SSYX oral administration. Results： Compared to the pacing group, the parameters of heart rate variability were lower after 8 weeks in the pacing ＋ SSYX group （low-frequency [LF] component： 20.85± 3.14 vs. 15.3±1.89 ms2, P =0.004; LF component/high-frequency component： 1.34 ± 0.33 vs. 0.77± 0.15, P 〈 0.001 ）. The atrial effective refractory period （AERP） was shorter and the dispersion of the AERP was higher after 8 weeks in the pacing group, while the changes were suppressed by SSYX intake. The dogs in the pacing group had more episodes and longer durations of AF than that in the pacing ＋ SSYX group. SSYX markedly inhibited the increase in sympathetic nerves and upregulation of tumor necrosis factor-alpha and interleukin-6 expression in the pacing ＋ SSYX group. Furthermore, SSYX suppressed the decrease of acetylcholine and α7 nicotinic acetylcholine receptor protein induced by long-term intermittent atrial pacing. Conclusions： SSYX substantially prevents atrial electrical remodeling and the progression of AF. These effects of SSYX may have association with regulating the imbalance of autonomic nerve activity and the cholinergic anti-inflammatory pathway.展开更多
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.
基金supported by grants from the National Natural Science Foundation of China(No. 81373743)Outstanding Young Talents Support Program of Anhui(No. 20140181)
文摘Objective： Acupuncture has a definite therapeutic effect on chronic obstructive pulmonary disease （COPD）, and the cholinergic anti-inflammatory pathway （CAP） has been shown to be involved in regula- tion of inflammation. In this study, we investigated whether electro-acupuncture （EA） affects the CAP in COPD,Methods： Sprague-Dawley rats were induced into COPD through exposure to cigarette smoke combined with lipopolysaccharide. EA treatment was applied at Zusanli （ST36） and Feishu （BL13） points for 30 min/d for 7 d. Seventy-two rats were randomly divided into six study groups, including normal, normal ＋ EA, normal ＋ α-bungarotoxin （α-BGT） （the antagonist of the nicotinic acetylcholine receptor α7 subunit （α7nAChR）） ＋ EA, COPD, COPD ＋ EA, and COPD ＋ α-BGT ＋ EA. Lung function, pathology and vagus nerve discharge were tested. The levels of acetylcholine （ACh）, acetylcholinesterase （ACHE）, interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-ct） in bronchoalveolar lavage fluid （BALF） and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA and protein expression and immunoreac- tivity of α7nAChR and its postreceptor inflammation signal pathway, including janus kinase 2 （JAK2）, sig- nal transducers and activators of transcription 3 （STAT3）, nuclear factor-KB （NF-KB）, were observed by quantitative reverse transcription-polymerase chain reaction, Western blot and immunohistochemistry. Results： Compared with normal rats, there were a significant decline in lung function and discharge of the vagus nerve （P 〈 0.01）, a marked sign of lung inflammation and an increase of ACh, ACHE, IL-6 and TNF-α level in BALF or lung tissue （P 〈 0.05, P 〈 0.01 ） and higher expression of 0t7nAChR, JAK2, STAT3 and NF-αB （P 〈 0.05, P 〈 0.01） in the COPD rats. In rats receiving EA, the lung function and vagal discharge were enhanced （P 〈 0.01 ）, lung inflammation was improved and the levels of ACh, ACHE, IL-
文摘Background： Shensong Yangxin （SSYX）, a traditional Chinese herbal medicine, has long been used clinically to treat arrhythmias in China. However, the mechanism of SSYX on atrial fibrillation （AF） is unknown. In this study, we tested the hypothesis that the effect of SSYX on the progression of paroxysmal AF is correlated with the regulation of autonomic nerve activity. Methods： Eighteen mongrel dogs were randomly divided into control group （n = 6）, pacing group （n = 6）, and pacing ＋ SSYX group （n = 6）. The control group was implanted with pacemakers without pacing; the pacing group was implanted with pacemakers with long-term intermittent atrial pacing; the pacing ＋ SSYX group underwent long-term intermittent atrial pacing and SSYX oral administration. Results： Compared to the pacing group, the parameters of heart rate variability were lower after 8 weeks in the pacing ＋ SSYX group （low-frequency [LF] component： 20.85± 3.14 vs. 15.3±1.89 ms2, P =0.004; LF component/high-frequency component： 1.34 ± 0.33 vs. 0.77± 0.15, P 〈 0.001 ）. The atrial effective refractory period （AERP） was shorter and the dispersion of the AERP was higher after 8 weeks in the pacing group, while the changes were suppressed by SSYX intake. The dogs in the pacing group had more episodes and longer durations of AF than that in the pacing ＋ SSYX group. SSYX markedly inhibited the increase in sympathetic nerves and upregulation of tumor necrosis factor-alpha and interleukin-6 expression in the pacing ＋ SSYX group. Furthermore, SSYX suppressed the decrease of acetylcholine and α7 nicotinic acetylcholine receptor protein induced by long-term intermittent atrial pacing. Conclusions： SSYX substantially prevents atrial electrical remodeling and the progression of AF. These effects of SSYX may have association with regulating the imbalance of autonomic nerve activity and the cholinergic anti-inflammatory pathway.
