Study on the Specific Expression of Infrared Radiation Temperature on the Body Surface of Acupoint in Rats with Chronic Myocardial Ischemic Injury.

BACKGROUND: Infrared thermal imaging technology was used to observe the changes in infrared radiation temperature at acupoints in rats caused by chronic myocardial ischemia injury. OBJECTIVE: This study aims to compare the difference of body surface infrared radiation temperature information of three groups of acupoints: bilateral Neiguan (PC6), bilateral Yanglingquan (GB33), and bilateral Sham Acupoints (SA) in the pathological state of myocardial ischemia injury, and to explore the relationship between acupoints and viscera state. METHODS: SPF adult Wistar male rats (n = 20) were randomly divided into a control (CTL; n = 10) and an isoproterenol group (ISO; n = 10). Chronic myocardial injury was induced in rats by subcutaneous injection of isoproterenol hydrochloride for 14 d. On the second day after the establishment of the model, the serum levels of cardiac troponin (cTnI) and creatine kinase isoenzyme (CK-MB) were measured by enzyme-linked immunosorbent assay (ELISA). The morphological changes of the myocardial tissue in the two groups were observed by hematoxylin-eosin (HE) staining and their pathological scores were evaluated, which was then used to determine the myocardial ischemic injury. Two days before and after the establishment of the model, the electrocardiograms (ECG) of the two groups of rats were recorded by the (ECG) data acquisition system, and the infrared thermal imaging platform was used to detect the temperature of the six acupoints. RESULTS: 1. After subcutaneous injection of isoproterenol hydrochloride for 14 days, the ST segment of the ECG decreased in the ISO group compared with that of the CTL group; 2. Myocardial tissue injury was serious in the ISO group compared to the CTL group; 3. Serum cTn-I and CK-MB were significantly increased (P <0 01) in the ISO group, compared to that in the CTL group; 4. The infrared radiation temperature on the body surface of bilateral Neiguan (PC6) acupoints decreased significantly in the ISO group, compared to that of the CTL group. CONCLUSION: Infrared thermal imaging technology can be used to detect the changes in the energy state of acupoints. Chronic myocardial ischemic injury can cause a decrease in IR temperature on the body surface of bilateral Neiguan (PC6) acupoints, suggesting that visceral diseases can lead to changes in the energy metabolism of acupoints.

Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis.

BACKGROUND: Myocardial fibrosis changes the structure of myocardium, leads to cardiac dysfunction and induces arrhythmia and cardiac ischemia, threatening patients' lives. Electroacupuncture at PC6 (Neiguan) was previously found to inhibit myocardial fibrosis. Long non-coding RNAs (lncRNAs) play a variety of regulatory functions in myocardial fibrosis, but whether electroacupuncture can inhibit myocardial fibrosis by regulating lncRNA has rarely been reported. METHODS: In this study, we constructed myocardial fibrosis rat models using isoproterenol (ISO) and treated rats with electroacupuncture at PC6 point and non-point as control. Hematoxylin-eosin, Masson and Sirius Red staining were performed to assess the pathological changes and collagen deposition. The expression of fibrosis-related markers in rat myocardial tissue were detected by RT-qPCR and Western blot. Miat, an important long non-coding RNA, was selected to study the regulation of myocardial fibrosis by electroacupuncture at the transcriptional and post-transcriptional levels. In post-transcriptional level, we explored the myocardial fibrosis regulation effect of Miat on the sponge effect of miR-133a-3p. At the transcriptional level, we studied the formation of heterodimer PPARG-RXRA complex and promotion of the TGF-ß1 transcription. RESULTS: Miat was overexpressed by ISO injection in rats. We found that Miat can play a dual regulatory role in myocardial fibrosis. Miat can sponge miR-133a-3p in an Ago2-dependent manner, reduce the binding of miR-133a-3p target to the 3'UTR region of CTGF mRNA and improve the protein expression level of CTGF. In addition, it can also directly bind with PPARG protein, inhibit the formation of heterodimer PPARG-RXRA complex and then promote the transcription of TGF-ß1. Electroacupuncture at PC6 point, but not at non-points, can reduce the expression of Miat, thus inhibiting the expression of CTGF and TGF-ß1 and inhibiting myocardial fibrosis. CONCLUSION: We revealed that electroacupuncture at PC6 point can inhibit the process of myocardial fibrosis by reducing the expression of lncRNA Miat, which is a potential therapeutic method for myocardial fibrosis.

Electroacupuncture at PC6 (Neiguan) Attenuates Angina Pectoris in Rats with Myocardial Ischemia-Reperfusion Injury Through Regulating the Alternative Splicing of the Major Inhibitory Neurotransmitter Receptor GABRG2.

Angina pectoris is the most common manifestation of coronary heart disease, causing suffering in patients. Electroacupuncture at PC6 can effectively alleviate angina by regulating the expression of genes, whether the alternative splicing (AS) of genes is affected by acupuncture is still unknown. We established a rat model of myocardial ischemia-reperfusion by coronary artery ligation and confirmed electroacupuncture alleviated the abnormal discharge caused by angina pectoris measured in EMG electromyograms. Analysis of the GSE61840 dataset established that AS events were altered after I/R and regulated by electroacupuncture. I/R decreased the expression of splicing factor Nova1 while electroacupuncture rescued it. Further experiments in dorsal root ganglion cells showed Nova1 regulated the AS of the GABRG2, specifically on its exon 9 where an important phosphorylation site is present. In vivo, results also showed that electroacupuncture can restore AS of GABRG2. Our results proved that electroacupuncture alleviates angina results by regulating alternative splicing.

The influence of pH and enzyme cross-linking on protein delivery properties of WPI-beet pectin complexes.

The incorporation of bioactive proteins and peptides into food is associated with the loss of bioactivity due to deactivation in complex food matrices and in digestion systems. In this study, two different types of protein carriers, i.e. biopolymer complexation and complex coacervation were fabricated using whey protein isolation (WPI, 6wt%) and beet pectin (BP, 1.25 and 1.00wt%) at pH5.5 and 3.5, respectively. The release of the encapsulated FITC-BSA, a model bioactive protein, in both carriers in the absence and presence of laccase was investigated at both pH7.0 and 4.0. Release of FITC-BSA from both lyophilized WPI-beet pectin biopolymer complexation and complex coacervation were biphasic with an initial burst release followed by a slower release phase. The addition of laccase in biopolymer complexation increased the loading efficiency from 44.95% to 52.15% and slowed down the burst release of FITC-BSA but did change the biphasic release pattern. Laccase-cross linked WPI (6wt%)-BP (1wt%) complex coacervation had highest FITC-BSA loading efficiency (96.90%). The release of the embedded FITC-BSA in this carrier at both pH4 and 7 was in a gradual manner and the profile can be fit to zero order kinetics over the 72h study period suggesting enzymatically reinforced complex coacervation between the protein and the negatively charged beet pectin can restrain the burst release of FITC-BSA. These results indicate that laccase cross-linked WPI-beet pectin complex coacervation can be a good carrier system for delivering hydrophilic bioactive proteins or peptides successfully with enhanced loading parameters and sustained release profiles.

Effects of high pressure treatment and temperature on lipid oxidation and fatty acid composition of yak (Poephagus grunniens) body fat.

Effects of high-pressure treatment (100 MPa to 600 MPa) on lipid oxidation and composition of fatty acids in yak body fat at 4 °C and 15 °C were investigated for up to 20 days storage. 400 and 600 MPa treatments increase the level of thiobarbituric acid-reactive substances (TBARS) 335% and 400% (p<0.05), respectively. Composition analysis shows that 600 MPa treatment induces a lower (p<0.05) percentage of polyunsaturated fatty acids, and C22:6 decreased significantly. A significant decrease in PUFA/SFA and n-6/n-3 PUFA values was observed at the end of storage. Samples treated at the lower pressures gave good sensory acceptability. It is concluded that a higher-pressure treatment is important in catalyzing lipid oxidation and the evolution of fatty acids in pressure-treated yak body fat.

[In vitro antitumor activities and mechanisms of galactosylated artemisinin].

OBJECTIVE: To explore the antitumor activities of galactosylated artemisinin in vitro and the related mechanisms. METHODS: Apoptosis rate of Hela cell was evaluated by using flow cytometry (FCM) analysis. The activity of Caspase-3 was examined by colorimetry. The expression level of p53, BAX, Caspase-3 and BCL-2 was determined by Western blotting. RESULTS: The FCM data showed that galactosylated artemisinin induced apoptosis of Hela cell. The activity and expression level of Caspase-3 were significantly increased when treated with galactosylated artemisinin for 36 h and 72 h. The expression of BAX was also increased markedly, while BCL-2 was reduced after treatment with the drug. However, galactosylated artemisinin had no effects on the expression of p53. CONCLUSION: Galactosylated artemisinin exhibits great antitumor activities, which may be ralated to triggering cytochrome C apoptotic pathway which mediated by BCL-2 family.