Points - Recent Research
Mast Cell Degranulation and Adenosine Release: Acupoint Specificity for Effect of Electroacupuncture on Pituitrin-Induced Acute Heart Bradycardia in Rabbits
Meta-Analysis of Randomized Controlled Trials of the Effects of Tai Chi on Blood Pressure
Lian Hua Qing Wen Capsules, a Potent Epithelial Protector in Acute Lung Injury Model, Block Proapoptotic Communication Between Macrophages, and Alveolar Epithelial Cells

Mast Cell Degranulation and Adenosine Release: Acupoint Specificity for Effect of Electroacupuncture on Pituitrin-Induced Acute Heart Bradycardia in Rabbits

Xuezhi Wang, et al.

Abstract
Acupuncture is a medical modality based on the theory of traditional Chinese medicine, and its effect is relatively dependent on acupoint specificity. However, there is little knowledge on acupoint specificity versus acupuncture outcomes because of the deficiency of rigorous investigation on this topic, which has impeded the growing legitimacy of acupuncture in the mainstream of medicine as an evidence-based therapy. Therefore, it is of utmost importance to clarify this critical issue. The present study aims to verify the phenomenon of acupoint specificity in acupuncture-induced cardiovascular regulation and explore the biological mechanism by measuring mast cells' degranulation and adenosine release. This study was conducted to explore the specificity of acupoints in an acute bradycardia rabbit model. After electroacupuncture (EA) stimulation at PC6, PC control (con) 1, PC con 2, LU7, LI11, and nonacupoint, only the PC6 group showed a significant improvement in relative heart rate as compared to that of the model group. There was no significant difference between the relative heart rate of other EA groups and that of the model group. Historical results also showed that the ratio of degranulated mast cells in PC6 was significantly higher than other acupoints and control points. From the results of high-performance liquid chromatography (HPLC), a transient elevation of adenosine concentration during EA was only observed on acupoints and control points (P < 0.05) along the pericardium meridian. The EA-induced adjustment on acute bradycardia exhibits a relative specificity of acupoints, which may be related to mast cell degranulation and adenosine release in local acupoint areas. Increased degranulation of mast cells and augmentation of adenosine release during EA may be the mechanisms for PC6 having significantly better acupuncture effects than other acupoints and nonacupoints.

Evid Based Complement Alternat Med. 2020; 2020: 1348914. Published online 2020 Oct 7. doi: 10.1155/2020/1348914

Source: PubMed

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Meta-Analysis of Randomized Controlled Trials of the Effects of Tai Chi on Blood Pressure

Xiaosheng Dong, et al.

Abstract
Abstract
Objectives: The purpose of this study was to investigate the influences of Tai Chi on blood pressure (BP) using the meta-analysis.
Methods: This paper used 6 e-resource databases, and randomized controlled trials on the role of Tai Chi on blood pressure were retrieved. Besides, the meta-analysis was conducted according to the guidelines of the Moose-recommendations and applied with Review Manager 5.3, and the risk of bias assessment was performed with the Cochrane Collaboration's tool. The inclusion, data extraction, and risk of bias assessment were independently finished by two researchers.
Results: There are 24 trials meeting the criteria of inclusion and the results were reviewed. The meta-analysis indicates that, compared with no exercise, Tai Chi had the influence of lowering systolic blood pressure (mean difference = −6.07, 95%CI (−8.75, −3.39), P < 0.00001) and diastolic blood pressure (mean difference MD = −3.83, 95%CI (−4.97, −2.69), P < 0.00001). No significant discrepancies in all outcomes between Tai Chi and other aerobic exercises were discovered.
Conclusion: Tai Chi can significantly reduce systolic and diastolic pressure than inactivity. However, Tai Chi does not show advantages in reducing blood pressure compared to other aerobic exercises.

Evid Based Complement Alternat Med. 2020; 2020: 8503047. Published online 2020 Oct 7. doi: 10.1155/2020/8503047

Source: PubMed

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Lian Hua Qing Wen Capsules, a Potent Epithelial Protector in Acute Lung Injury Model, Block Proapoptotic Communication Between Macrophages, and Alveolar Epithelial Cells

Qi Li, et al.

Abstract
Abstract
Besides pathogen evading, Acute Lung Injury (ALI), featuring the systematic inflammation and severe epithelial damages, is widely believed to be the central non-infectious factor controlling the progression of infectious diseases. ALI is partly caused by host immune responses. Under the inspiration of unsuccessful treatment in COVID-19, recent insights into pathogen–host interactions are leading to identification and development of a wide range of host-directed therapies with different mechanisms of action. The interaction unit consisting of macrophages and the alveolar epithelial cells has recently revealed as the therapeutic basis targeting ALI. Lian Hua Qing Wen capsule is the most effective and commonly-used clinical formula in treating respiratory infection for thousands of years in China. However, little is known about its relevance with ALI, especially its protective role against ALI-induced alveolar tissue damages. Aiming to evaluate its contribution in antibiotics-integrating therapies, this study pharmacologically verified whether LHQW could alleviate lipopolysaccharide (LPS)-induced ALI and explore its potential mechanisms in maintaining the physiology of macrophage-epithelial unit. In ALI mouse model, the pathological parameters, including the anal temperature, inflammation condition, lung edema, histopathological structures, have all been systematically analyzed. Results consistently supported the effectiveness of the combined strategy for LHQW and low-dose antibiotics. Furthermore, we established the macrophages-alveolar epithelial cells co-culture model and firstly proved that LHQW inhibited LPS-induced ER stress and TRAIL secretion in macrophages, thereby efficiently protected epithelial cells against TRAIL-induced apoptosis. Mechanistically, results showed that LHQW significantly deactivated NF-κB and reversed the SOCS3 expression in inflammatory macrophages. Furthermore, we proved that the therapeutic effects of LHQW were highly dependent on JNK-AP1 regulation. In conclusion, our data proved that LHQW is an epithelial protector in ALI, implying its promising potential in antibiotic alternative therapy.

Front Pharmacol. 2020; 11: 522729. Published online 2020 Sep 23. doi: 10.3389/fphar.2020.522729

Source: PubMed

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