Artemisia argyi Lev. et Vant. (A. argyi) is widely utilized for moxibustion in Chinese medicine, and the mechanism underlying terpenoid biosynthesis in its leaves is suggested to play an important role in its medicinal use. However, the A. argyi transcriptome has not been sequenced. Herein, we performed RNA sequencing for A. argyi leaf, root and stem tissues to identify as many as possible of the transcribed genes. In total, 99,807 unigenes were assembled by analysing the expression profiles generated from the three tissue types, and 67,446 of those unigenes were annotated in public databases. We further performed differential gene expression analysis to compare leaf tissue with the other two tissue types and identified numerous genes that were specifically expressed or up-regulated in leaf tissue. Specifically, we identified multiple genes encoding significant enzymes or transcription factors related to terpenoid synthesis. This study serves as a valuable resource for transcriptome information, as many transcribed genes related to terpenoid biosynthesis were identified in the A. argyi transcriptome, providing a functional genomic basis for additional studies on molecular mechanisms underlying the medicinal use of A. argyi.

The hippocampus is involved in the regulation of the autonomic nervous system, together with the hypothalamus and brainstem nuclei, such as the paraventricular nucleus and nucleus tractus solitarius. The vagus nerve-nucleus tractus solitarius pathway has an important role in cardiovascular reflex regulation. Myocardial ischemia has been shown to cause changes in the autonomic nervous system, affecting the dynamic equilibrium of the sympathetic and vagal nerves. However, it remains poorly understood how the hippocampus communicates with brainstem nuclei to regulate the autonomic nervous system and alleviate myocardial ischemic tissue damage. A rat model of acute myocardial ischemia (AMI) was made by ligating the left anterior descending branch of the coronary artery. Three days before ischemia, the hippocampal CA1 region was damaged. Then, 3 days after ischemia, electroacupuncture (EA) at Shenmen (HT7)-Tongli (HT5) was performed (continuous wave, 1 mA, 2 Hz, duration of 30 minutes). Cluster analysis of firing patterns showed that one type of neuron was found in rats in the sham and AMI groups. Three types of neurons were observed in the AMI + EA group. Six types of neurons were found in the AMI + EA + Lesion group. Correlation analysis showed that the frequency of vagus nerve discharge in each group was negatively correlated with heart rate (HR) (P < 0.05, r = −0.424), and positively correlated with mean arterial pressure (MAP) (P < 0.05, r = 0.40987) and the rate-pressure product (RPP) (P < 0.05, r = 0.4252). The total frequency of the nucleus tractus solitarius discharge in each group was positively correlated with vagus nerve discharge (P < 0.01, r = 0.7021), but not with hemodynamic index (HR: P > 0.05, r = −0.03263; MAP: P > 0.05, r = −0.08993; RPP: P > 0.05, r = −0.03263). Some neurons (Neuron C) were negatively correlated with vagus nerve discharge, HR, MAP and RPP in the AMI + EA group (vagus nerve discharge: P < 0.05, r = −0.87749; HR: P < 0.01, r = −0.91902; MAP: P < 0.05, r = −0.85691; RPP: P < 0.01, r = −0.91902). Some neurons (Neurons C, D and E) were positively correlated with vagus nerve discharge, HR, MAP and RPP in the AMI + EA + Lesion group (vagus nerve discharge: P < 0.01, r = 0.8905, P < 0.01, r = 0.9725, P < 0.01, r = 0.9054; HR: P < 0.01, r = 0.9347, P < 0.01, r = 0.9089, P < 0.05, r = 0.8247; MAP: P < 0.05, r = 0.8474, P < 0.01, r = 0.9691, P < 0.01, r = 0.9027; RPP: P < 0.05, r = 0.8637, P < 0.01, r = 0.9407, P < 0.01, r = 0.9027). These findings show that the hippocampus-nucleus tractus solitarius-vagus nerve pathway is involved in the cardioprotective effect of EA at the heart meridian. Some interneurons in the nucleus tractus solitarius may play a particularly important role in the cardiomodulatory process.

Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressure product, were apparently impaired after AMI injury. By contrast, EA stimulating could ameliorate the impairments of heart function (P<0.05). Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA. Neuronal activity in CA1 area was affected by AMI. As evidenced, cell counts, cell types, and frequency of the discharged neurons were facilitated after AMI, while EA stimulation attenuated the abnormalities. Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation. Correlations were established between c-Fos expression and cell counts of discharged neurons, as well as between heart function and cell counts of discharged neurons. Taken together, EA stimulation at heart meridian protects against heart dysfunction induced by AMI possibly through suppressing the neuronal activity in CA1 region.

The optimum dose of isoprenaline (ISO) required to induce stress cardiomyopathy (SC) in mice is not known. The present study aimed to investigate the dose‑response association and determine the optimum dose of ISO to establish a high‑morbidity/low‑mortality SC mouse model to simulate the clinical symptoms of SC. A total of 72 6‑week‑old wild‑type female mice (C57BL/6) were randomly divided into control mice administered normal saline and mice treated with increasing ISO concentrations (5, 10, 25, 50 and 100 mg/kg ISO intraperitoneal injections daily for 14 consecutive days). All mice were analysed by body weight assessment, open field test (OFT), echocardiography (Echo), electrocardiogram (ECG), assessment of myocardial pathology and quantification of cortisol, brain natriuretic peptide (BNP), cardiac troponin T (cTnT), catecholamine (CA) and C‑reactive protein (CRP). Compared with the control group, the 25 and 50 mg/kg ISO groups exhibited the most prominent weight changes and lower mortality. The open‑field test showed a significant decrease in autonomous activity behaviour in the 25 and 50 mg/kg ISO groups compared with the control group (P<0.05). Echo revealed that the apex of the heart was balloon‑like in the 25 and 50 mg/kg ISO groups, along with prominent left ventricular dyskinesia. ECG showed a significant increase in ST segment amplitude, QT interval and Q amplitude (P<0.05) in the 25 and 50 mg/kg ISO group compared with the control group. Haematoxylin and eosin staining of heart tissue showed a disordered arrangement of myocardial cells, dissolution of myocardial fibres and cytoplasm, notable widening of myocardial cell space, oedema and hyperaemia of the interstitium, whereas heart tissue of the control group was structurally intact. Compared with the control group, the 25 and 50 mg/kg ISO groups exhibited significantly higher levels of cortisol, BNP, cTNT, CA and CRP (P<0.05). A high‑incidence low‑mortality SC model was successfully and stably developed by administration of 25 and 50 mg/kg ISO. Such models may provide a basis for the development of other animal models of SC.