RÉSUMÉ
Objective: By sorting and analyzing pertinent modern studies targeting auricular point therapy treating primary insomnia (PI), to summarize the point selection rules and clinical efficacy of using auricular points alone or combining it with other therapies in treating PI. Methods: A search on China National Knowledge Infrastructure (CNKI), Wanfang Academic Journal Full-text Database (Wanfang), Chongqing VIP Database (CQVIP), PubMed, Springer and Ovid were conducted from January 1, 1998 till January 31, 2020. Point selection, diagnostic criteria and Pittsburgh sleep quality index (PSQI) in the eligible studies were analyzed and summarized. Results: The difference in PSQI before and after using auricular point therapy alone was more significant than that of using Chinese medication alone (P<0.05), but less significant than that of combining auricular point therapy and acupuncture-moxibustion and Chinese therapeutic massage (tuina) (P<0.05). In the included studies, Shenmen (TF4) was the most commonly used (370 times), followed by Heart (CO15), which was 344 times, and Subcortex (AT4), which was 325 times. In terms of auricular points distribution, points in the auricular concha were the most commonly used (1500 times), followed by those in the antitragus (474 times) and triangular fossa (387 times). Correlation analysis showed that Shenmen (TF4) and Liver (CO12), Sympathetic (AH6a) and Heart (CO15) were used together more often, followed by Shenmen (TF4), Liver (CO12), Spleen (CO13), Kidney (CO10) and Subcortex (AT4), and then Shenmen (TF4), Liver (CO12), Sympathetic (AH6a), Subcortex (AT4) and Heart (CO15). Cluster analysis showed that the auricular points used for PI can be divided into 6 clusters in 2 major groups. One group was Heart (CO15), Subcortex (AT4), Shenmen (TF4), Sympathetic (AH6a), Spleen (CO13), Kidney (CO10), Liver (CO12) and Endocrine (CO18); the other was Occiput (AT3), Stomach (CO4), Pancrease-gallbladder (CO11), Chuiqian (LO4), Small Intestine (CO6), Central Rim (AT2,3,4i) and Sanjiao (CO17). In terms of patterns in traditional Chinese medicine, the pattern of dual deficiency of heart and spleen accounted for the largest proportion in the studies of using auricular points alone or combining it with other treatments to treatment PI, and then it was the pattern of liver depression transforming into fire. Conclusion: In treatment of PI with auricular points alone or combo therapy involving auricular points, Shenmen (TF4) was commonly used, and the commonly used point group consisted of Shenmen (TF4), Liver (CO12), Sympathetic (AH6a) and Heart (CO15). Auricular point therapy can be taken as a complementary therapy in treating PI.
RÉSUMÉ
This study was purposed to investigate the inhibitory effect of bactericidal permeability-increasing protein (BPI) on lipopolysaccharide (LPS)-mediated activation of platelets. Venous blood samples were obtained from 10 healthy volunteers and were prepared into platelet-rich plasma (PRP, 1 × 10(8)/ml). Experiments were divided into four groups: normal platelet group (untreated group); LPS group, BPI group and BPI+LPS group. PRP were stimulated by LPS (10 µg/ml) in the presence and absence of BPI (100 µg/ml) or BPI alone. Then platelets were harvested and determined for Toll-like receptor-4 (TLR-4) with flow cytometry (FCM), the supernatant was used for detection of cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) with enzyme-linked immunosorbent assay (ELISA). The results showed that as compared with normal platelet group, TLR-4 expression on platelets was significantly increased under LPS stimulation (P < 0.001); the levels of TNF-α and IL-6 in the supernatant were also remarkably elevated (P < 0.001). However, either TLR-4 expression or the cytokine levels significantly decreased in the presence of BPI when platelets underwent LPS-challenge (P < 0.05), but still were higher than that in normal platelet group. Stimulating the platelets with BPI alone could not enhance the TLR-4 expression and cytokine levels. It is concluded that BPI has the ability to inhibit the LPS-induced platelet activation.
Sujet(s)
Humains , Peptides antimicrobiens cationiques , Pharmacologie , Protéines du sang , Pharmacologie , Inflammation , Lipopolysaccharides , Activation plaquettaire , Plasma riche en plaquettes , Métabolisme , Récepteur de type Toll-4 , MétabolismeRÉSUMÉ
The study was aimed to investigate the expression of Toll-like receptor 4 (TLR4) on platelets and to determine whether platelet TLR4 involves in its activation induced by lipopolysaccharide (LPS). Human platelet-rich plasma (PRP) and platelet suspension obtained from 15 healthy individuals pretreated with a concentration of 0.2 microg/ml of LPS in the presence or absence of thrombin (1 U/ml) for 1 hour. The expressions of TLR4, CD62P (P-select) and CD40L on platelets were detected by flow cytometry, and platelet TLR4 expression was further determined by Western blot analysis. The results indicated that the percentage of TLR4-positive platelets induced by thrombin was increased by 32.34% compared with the resting platelets (25.44%, p < 0.05). TLR4 expression on platelets treated with LPS was remarkably elevated in the presence or absence of thrombin. However, the expression level of the former was much higher than that of the latter and thrombin stimulation alone (p < 0.05). Moreover, the similar results were found in Western blot analysis. Synchronously, expressions of CD62P and CD40L on resting platelets were 6.39% and 2.45%, they were also markedly increased when treated with thrombin (42.68% and 14.8%) and LPS respectively, and the increases of expression of CD62P and CD40L were more significant when stimulated with both LPS and thrombin (63.03% and 13.94%). Although anti-TLR4 antibody inhibited significantly the increase of TLR4, CD62P and CD40L on platelets induced by LPS, which did not affect their increase induced by thrombin. In conclusion, the evidence has been shown that functional TLR4 can be expressed on human platelets. It may involve in platelet activation as an important mediator of LPS-induced CD62P and CD40L expressions on platelets.