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Ischemic stroke is caused by a variety of factors caused by intracerebral artery stenosis or obstruction， can lead to cerebral ischemia， hypoxia， neuronal necrosis and neurological dysfunction and other pathological injuries， with high morbidity， high disability rate， high mortality characteristics. Cerebral ischemia-reperfusion injury is the main secondary injury， which can lead to permanent disability or even death in severe cases. With the development of traditional Chinese medicine（TCM） modernization， the extraction and application of active components of TCM have been paid more and more attention. Salidroside， as the main active component of Rhodirosea， a rare Chinese medicinal herb， has been proved to fight cerebral ischemia injury by inhibiting cell apoptosis， anti-oxidative stress， reducing inflammatory response， protecting blood-brain barrier， regulating autophagy， promoting nerve remodeling and synaptic regeneration in preclinical trials. However， due to its multi-pathway， multi-pathway and multi-target action characteristics， the specific mechanism of salidroside to improve cerebral ischemia injury has not been fully elucidated. By reviewing relevant literature in the past decade， the author reviewed the mechanism of action of salidroside in the treatment of ischemic brain injury， and summarized the recent progress of its pharmacokinetic studies and safety evaluation， in order to provide theoretical basis and new research ideas for the development and clinical application of the active ingredients of traditional Chinese medicine.
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OBJECTIVE: To investigate the effect of electroacupuncture (EA) on the expression of interleukin-8 (IL-8), interleukin-10 (IL-10), tyrosine hydroxylase (TH), β3-adrenergic receptor (β3AR), and endothelial nitric oxide synthase (eNOS) in myocardial tissue in ischemic myocardial injury rats, so as to reveal its underlying mechanisms in myocardial protection via anti-inflammation and sympathetic nerve remodeling. METHODS: A total of 48 male Sprague-Dawley rats were randomly divided into sham-operation (sham, n＝9), sham ＋EA (n＝9), model (n＝15) and EA (n＝15) groups. The myocardial ischemia (MI) model was established by ligation of the left anterior descending branch of the left coronary artery. EA (2 Hz/15 Hz，1.5－2 mA) was applied to bilateral "Neiguan" (PC6) for 30 min, once daily for 4 days. The myocardial infarct size was detected by 2, 3, 5 triphenyltetrazolium chloride (TTC) staining, myocardial histopathological changes and inflammatory infiltration were assessed by H．E. staining, and the expression of IL-8, IL-10, TH, β3AR, and eNOS in the myocardium was determined by using Western blot. RESULTS: Compared with the sham group, a marked myocardial infarction was found in the left ventricle tissue, accompanied with disordered arrangement of myocardial fibers and higher degree of inflammatory cell infiltration, and increased expression of IL-8, TH, β3AR and eNOS in the myocardium in the model group (P0.05). After EA intervention and in comparison with the model group, the myocardial infarct size was significantly reduced (P<0.01), the severity of inflammatory cell infiltration and disordered arrangement of myocardial fibers were relieved, and the expression of IL-10 and eNOS proteins were significantly up-regulated (P<0.05), and the markedly up-regulated expression of IL-8, TH, and β3AR were significantly suppressed in the EA group (P<0.01)．. CONCLUSION: EA intervention can reduce the myocardial infarct size (protective effect) in MI rats possibly by reducing inflammatory reaction and sympathetic nerve remodeling.
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Objective: To observe the impact of high thoracic epidural blockade (HTEB) on atrial autonomic nerve remodeling in dogs with atrial ifbrillation (AF) induced by long-term rapid right atrial appendage pacing and to explore the effect of nerve growth factor (NGF) on atrial autonomic nerve remodeling. Methods: AF model was established by consistent rapid atrial pacing for 6 weeks. 18 experimental dogs were randomly divided into 3 groups: Sham group, the dogs had no pacing while received normal saline injection; Control group, the dogs had pacing and normal saline injection; HTEB group, the dogs had pacing and 0.5% lidocaine injection for HTEB.n=6 in each group. Atrial myocardium collagen volume fraction (CVF) was examined by Masson staining; sprouting of NGF related protein 43 (GAP43) and tyrosine hydroxylase (TH) were assessed by immunohistochemistry; protein expressions of NGF, GAP43 and TH were measured by Western blot analysis. Results: Compared with Sham group, HTEB group showed decreased CVF and sprouting of GAP43, TH,P Conclusion: Long-term rapid atrial pacing induced AF dog had inhomogeneous sprouting of atrial myocardial nerve which may cause autonomic nerve remodeling; NGF played the important role in such process. HTEB could effectively inhibit NGF up-regulation and suppress the autonomic nerve remodeling in experimental dogs.
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Objective To observe the effect of renal denervation (RDN) on the cardiac oxidative stress and sympathetic nerve remodeling after myocardial infarction (MI) in canine. Methods Canine (n=18) were randomly divided into three groups: Sham operation group (SHAM group, n=6), MI group (n=6), MI+RDN group (n=6). Anterior myocardial infarction was gained by gelatin sponge embolization of the left anterior descending artery. At four weeks post-MI, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and left ventricular ejection fraction (LVEF) were examined using echocardiography. Immunohistochemical assay was used to analyze the distribution and density of tyrosine hydroxylase (TH) stained nerve fibers at peri-infarct zone. Myocardial superoxide dismutase (SOD) activity and malondialde?hyde (MDA) were also assessed. Results Compared with dogs in SHAM group, LVEF and SOD expression were decreased in MI group and MI+RDN group (P<0.05), but Left ventricular end diastolic pressure (LVEDP), LVEDV, LVESV, MDA and rate of TH positive staining nerve fibers were increased (P<0.05). There was a negative correlation between the rate of TH positive staining nerve fibers and SOD level (rs=-0.818,P<0.05) and a positive correlation between rate of TH positive stain?ing nerve fibers with MDA level (rs=0.900,P<0.05). By contract, compared with MI group, LVEF and SOD in MI +RDN group were increased (P<0.05), while LVEDV, LVESV, MDA and rate of TH positive staining nerve fibers were significant?ly lowered (P<0.05). Conclusion RDN is effective to decrease the level of cardiac oxidative stress and improve cardiac sympathetic nerve remodeling and heart function after myocardial infarction in canine.
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Objective: To conifrm the omentopexy decreasing the susceptibility of ventricular arrhythmia in experimental rats with chronic myocardial infarction (MI) by nerve remodeling. Methods: The MI model of SD rats was established by left coronary artery ligation. 3 weeks later, the qualiifed animals were randomized into 3 groups for the 2nd operation. ① Sham operation group, the rats received the 2nd operation without ligation, ② Isolated MI group, the rats received the 2nd operation without omentopexy, ③ Omentopexy group, the rats received the 2nd operation with omentopexy. n=20 in each group. 4 weeks after the 2nd operation, the electrophysiological characteristics were assessed by relevant techniques, the new and sympathetic nerves in MI border zone were examined by immunohistochemistry, the protein expressions of connexin43 and nerve growth factor (NGF) were measured by western blot analysis and the cardiac endothelin-1 (ET-1) level was evaluated by ELISA. Results: Compared with Isolated MI group, Omentopexy group showed decreased susceptibility of arrhythmia (3.5 ± 1.2) vs (0.9 ± 0.2), improved electrical transduction (1.5 ± 0.2) mV vs (3.4 ± 0.3) mV and decreased capture threshold (5.5 ± 0.3) mV vs (2.2 ± 0.2) mV, all P Conclusion: Omentopexy may decrease the susceptibility of ventricular arrhythmia after MI in experimental rats, which might be related to the cardiac nerve remodeling.
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Aim To investigate the preventive effect of Guizhi decoction on cardiac sympathetic sprouting induced by 4-Methylcatechol (4-MC) . Methods The rat models of cardiac sympathetic sprouting were in-duced by 10 mg · L-1 4-MC ( 10μg · kg-1 body weight, i. p. ) . Guizhi decoctions ( with different pro-portion between Ramulus Cinnamomi and Radix Paeon-iae Alba, 1 : 1, 1 : 2 and 2 : 1) and metoprolol were administered to the rats. Heart rate and electrocardio-gram ( ECG ) were observed, the content of norepi-nephrine (NE), growth associated protein (GAP-43), tyrosine hydroxylase ( TH ) and acetylcholine transfer-ase enzyme ( CHAT) in myocardial homogenate of left ventricular and right atrial were determined by ELISA method, and immunofluorescence assay was used to observe cardiac nerve sprouting and sympathetic distri-bution. Results 4-MC caused cardiac sympathetic sprouting and parasympathetic was not influenced. Heart rate of the model group was improved significant-ly and higher than that of the other groups . Compared with the model group, the content of NE, GAP-43 and TH in left ventricle and right atrium of the metoprolol group and Guizhi decoction group were decreased( P<0.05 ) , and the immunofluorescence result showed that the distribution of TH positive nerve was reduced sig-nificantly(P<0.05). It was demonstrated that Guizhi decoction of the proportion between Ramulus Cinnamo-mi and Radix Paeoniae Alba 1 : 1 and 1 : 2 had the best efficacy, which was similar to the efficacy of meto-prolol. Conclusion Guizhi decoction ( with the pro-portion between Ramulus Cinnamomi and Radix Paeon-iae Alba 1 : 1 and 1 : 2 ) effectively inhibits the cardi-ac sympathetic sprouting induced by 4-MC.