Effect of electroacupuncture on inflammatory response and immune cells in mice with chronic inflammatory pain. / ç”µé’ˆå¯¹æ ¢æ€§ç‚Žæ€§ç—›å°é¼ ç‚Žæ€§ååº”å’Œå ç–«ç»†èƒžçš„å½±å“.

OBJECTIVES: To observe the effects of electroacupuncture(EA) on local inflammatory mediators and macrophage polarization, and immune cells in the spleen of mice with chronic inflammatory pain induced by complete Freund's adjuvant (CFA) in the hind paw, so as to investigate the immunoinflammatory regulatory mechanisms of EA in relieving pain and swelling in mice with chronic inflammatory pain. METHODS: Thirty C57BL/6 mice were randomly divided into control, model, and EA groups, with 10 mice in each group. Chronic inflammatory pain model were established by subcutaneous injection of 20 µL CFA solution in the left hind paw for 7 consecutive days. After modeling, mice in the EA group received EA at bilateral "Zusanli"(ST36) for 20 min (2 Hz/100 Hz, 1 mA) once a day for 18 consecutive days. Mechanical pain threshold, heat pain thresholds, and paw thickness were measured before and after mode-ling, and after interventions. Western blot was used to detect the expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, and NOD-like receptor protein 3 (NLRP3) in the paw tissue. Immunohistochemistry was used to detect the positive expression of M1-type macrophage marker inducible nitric oride synthase (iNOS) and M2-type marker CD206 in the paw, and flow cytometry was used to detect the proportion of F4/80+ CD11b+ macrophages, Ly6G+ CD11b+ neutrophils, and CD25+ Foxp3+ regulatory T cells (Treg) in the spleen. RESULTS: Compared with the control group, mechanical pain and heat pain thresholds were significantly reduced(P<0.000 1), while paw thickness, expressions of IL-1ß, TNF-α, and NLRP3 in the paw, and positive expression of M1 macrophage marker iNOS in the paw, the proportions of macrophages and neutrophils in the spleen were significantly increased (P<0.000 1, P<0.001) in the model group. Compared with the model group, mechanical pain threshold and heat pain thresholds, CD206 positive expression in the paw, and Treg cell proportion in spleen were significantly increased (P<0.01), while paw thickness, the expressions of IL-1ß, TNF-α and NLRP3 in the paw, as well as the positive expression of M1 macrophage marker iNOS in the paw, the proportions of macrophages and neutrophils in the spleen were significantly reduced (P<0.001, P<0.01, P<0.05)in mice of the EA group after intervention. CONCLUSIONS: EA may alleviate pain and swelling in mice with chronic inflammatory pain by regulating the numbers of macrophages, neutrophils, and Treg cells, as well as promoting M2 polarization of local macrophages and inhibiting the release of pro-inflammatory cytokines.

Genome-wide analysis in PC6 electroacupuncture to ameliorate carfilzomib-induced cardiotoxicity in mice.

Carfilzomib (CFZ), a proteasome inhibitor commonly used in the treatment of multiple myeloma (MM), exhibits limited clinical application due to its cardiotoxicity. In our study, electroacupuncture (EA) at Neiguan acupoint (PC6) effectively reversed CFZ-induced reduction in ejection fraction (EF) and fractional shortening (FS), demonstrating great potential effect for heart protection. Through comparative analysis of the transcriptome profile from heart samples of mice treated with DMSO control, CFZ injection, and EA stimulation, we identified a total of 770 differentially expressed genes (DEGs) in CFZ (vs. Control) group and 329 DEGs in EA (vs. CFZ) group. Specifically, CFZ (vs. Control) group exhibited 65 up-regulated DEGs and 705 down-regulated DEGs, while EA (vs. CFZ) group displayed 251 up-regulated DEGs and 78 down-regulated DEGs. Metascape analysis revealed that among these treatment groups, there were 137 co-expressed DEGs remarkably enriched in skeletal system development, cellular response to growth factor stimulus, negative regulation of Wnt signaling pathway, and muscle contraction. The expression patterns of miR-8114, Myl4, Col1a1, Tmem163, Myl7, Sln, and Fxyd3, which belong to the top 30 DEGs, were verified by quantitative real-time PCR (RT-qPCR). In summary, this study firstly discloses novel insights into the regulatory mechanisms underlying PC6-based EA therapy against CFZ-induced cardiotoxicity, potentially serving as a theoretical foundation for further clinical applications.

[Effect of different electrical current intensities of electroacupuncture preconditioning on cardiac function and macrophage polarization in mice with acute myocardial ischemia].

OBJECTIVE: To observe the effect of different intensities of electroacupuncture (EA) preconditioning on car-diac function and polarization state of macrophages in mice with acute myocardial ischemia (AMI), so as to explore its possible mechanism underlying improvement of AMI. METHODS: A total of 50 male C57BL/6J mice were randomly divided into sham ope-ration, AMI model, and EA pretreatment groups (0.5 mA, 1 mA, 3 mA subgroups), with 10 mice in each group/subgroup. The mice in the EA pretreatment groups were subjected to EA stimulation of bilateral "Neiguan"(PC6) with 0.5, 1.0 and 3 mA respectively and frequency of 2 Hz/15 Hz for 20 min, once a day, for 3 days. The acute myocardial ischemia model was established by ligating the anterior descending branch (ADB) of the left coronary artery, while the sham operation only had a surgical suture trans-passed below the ADB but without ligation. The myocardial infarction area was measured after TTC staining, and the cardiac function ï¼»left ventricular ejection fraction (EF), short-axis contraction rate (FS)ï¼½ was detected by using echocardiography. The M1 macrophages were labeled with CD11b+F480+CD206low, M2 macrophages were labeled with CD11b+F480+CD206high and detected by using flow cytometry, and the expression levels of myocardial interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), Toll-like receptor-4 (TLR4) proteins were detected by using Western blot. RESULTS: Compared with the sham operation group, the model group had a significant increase in the infarction area (P<0.000 1), number of cardiac macrophages and percentage of M1 type macrophages (P<0.000 1), and the expression levels of myocardial IL-1ß, TNF-α, TLR4 proteins (P<0.001, P<0.01), and a remarkable decrease in the levels of EF, FS and the percentage of M2 type macrophages (P<0.000 1). In contrast to those of the model group, the area of myocardial infarction (P<0.000 1, P<0.01), expression levels of myocardial IL-1ß, TNF-α, TLR4 proteins (P<0.01, P<0.05, P<0.001) in the 0.5 mA, 1 mA and 3 mA groups, number of macrophages and percentage of M1 macrophages (P<0.05) in the 1 mA group were significantly decreased, while the levels of EF and FS (P<0.000 1, P<0.05, P<0.001) in the 3 EA groups, and percentage of M2 macrophage (P<0.05) in the 1 mA group were significantly increased. Comparison among the 3 EA groups displayed that the effects of 1 mA group were significantly superior to those of 0.5 and 3 mA groups in up-regulating EF and FS (P<0.01, P<0.001), and in down-regulating the area of infarct myocardium (P<0.01, P<0.000 1), and the expression of TLR4 protein (P<0.01), and 0.5 mA group in the expression of IL-1ß and TNF-α proteins (P<0.05). CONCLUSION: EA preconditioning with electrical current intensities of 0.5 mA, 1 mA and 3 mA can effectively reduce myocardial infarction size, improve cardiac function in mice with AMI, which may be related with its effects in reducing the number of cardiac macrophages and down-regulating the expression of myocardial IL-1ß, TNF-α and TLR4 proteins. The therapeutic effect of 1 mA is better than that of 0.5 and 3 mA.

Electroacupuncture interventions alleviates myocardial ischemia reperfusion injury through regulating gut microbiota in rats.

Electroacupuncture (EA) intervention has a remarkable cardioprotection against myocardial ischemia reperfusion injury (MIRI). Recently, it has been suggested that the gut microbiota plays an important role in regulating the progression and prognosis of MIRI. The purpose of this study was to illustrate the relationship between gut microbiota and cardioprotection of EA on MIRI. We conducted a MIRI model by ligating the left anterior descending coronary artery for 30 min followed by reperfusion in male Sprague Dawley rats, which then received 7 days of EA intervention. Echocardiography was employed to evaluate left ventricular function. Fecal samples were collected for microbial analysis by 16S rDNA high-throughput sequencing. Blood samples and myocardium were collected for inflammatory cytokine detection by enzyme linked immunosorbent assay (ELISA) and Western blot. Hematoxylin & eosin (HE) staining and immunofluorescence of ileum tissue were performed for intestinal damage evaluation. After 7 days of EA intervention, the left ventricular function was improved with significantly increased ejection fraction and fractional shortening. Furthermore, we found that EA intervention reversed the changed gut microbiota induced by MIRI, including Clostridiales, RF39, S24-7, Desulfovibrio, and Allobaculum, improved the impaired gut barrier, reduced the production and circulation of lipopolysaccharide (LPS), inhibited the level of interleukin 6 (IL-6) and interleukin 12 (IL-12) in periphery and decreased the expression of Toll like receptor 4 (TLR4) and IL-6 in myocardium. EA intervention could improve the impaired gut mucosal barrier and reduce the production and circulation of LPS after MIRI through regulating gut microbiota, thus inhibiting the circulation and myocardium inflammation and finally exerted the cardioprotective effect.

Electroacupuncture improves cardiac function and reduces infarct size by modulating cardiac autonomic remodeling in a mouse model of myocardial ischemia.

BACKGROUND: Sympathetic and parasympathetic nerve remodeling play an important role in cardiac function after myocardial ischemia (MI) injury. Increasing evidence indicates that electroacupuncture (EA) can regulate cardiac function by modulating the autonomic nervous system (ANS), but little is known about its effectiveness on neural remodeling post-MI. OBJECTIVES: To investigate the role of EA in ANS remodeling post-MI. METHODS: Adult male C57/BL6 mice were equally divided into the Control (Ctrl), MI and EA groups after generating the MI model by ligating the left anterior descending (LAD) coronary artery. Echocardiography and 2,3,5-triphenyltetrazolium (TTC) staining were employed to evaluate cardiac function and infarct size after EA treatment for five consecutive days. Serum norepinephrine (NE) levels were measured by ELISA to quantify sympathetic activation. Then, ANS remodeling was detected by immunohistochemistry (IHC), RT-qPCR, and Western blotting. RESULTS: Our preliminary findings showed that EA increased ejection fraction and fractional shortening and reduced infarct area after MI injury. Serum NE levels in the EA group were significantly decreased compared with those in the MI group. IHC staining results demonstrated that the density of growth associated protein (GAP)43 and tyrosine hydroxylase (TH) positive nerve fibers in the EA group were decreased with increased choline acetyltransferase (CHAT) and vesicular acetylcholine transporter (VACHT). Meanwhile, the results verified that mRNA and protein expression of GAP43 and TH were significantly inhibited by EA treatment in the MI mice, accompanied by elevated CHAT and VACHT. CONCLUSIONS: EA treatment could improve cardiac function and reduce infarct size by modulating sympathetic and parasympathetic nerve remodeling post-MI, thus helping the cardiac ANS reach a new balance to try to protect the heart from further possible injury.

Hydrothermal liquefaction of Chlorella pyrenoidosa and effect of emulsification on upgrading the bio-oil.

This work studied the hydrothermal liquefaction of Chlorella pyrenoidosa and effect of emulsification on upgrading the bio-oil. The fuel properties and storage stability characteristics of emulsion fuels were explored. The combustion characteristic analysis showed that the ignition temperatures of emulsion fuels (139.6-151.3 °C) were lower than that of bio-oil (176.9 °C). Besides, emulsion fuels had higher comprehensive combustion indexes (7.24-14.08 × 10-6 × min-2 × C-3) than bio-oil (1.51 × 10-6 × min-2 × C-3), indicating that emulsion fuels had better combustion performance. The kinetic analysis showed that emulsification could effectively reduce the activation energy, resulting in less energy input for combustion. Based on chemical composition evolution during the storage process, a possible stability mechanism was proposed. The storage stability analysis indicated that the diesel-solvable fractions in bio-oil had better stability. Overall, this work provides a feasible way for bio-oil upgrading through emulsification. In addition, a better understanding of the stability property of emulsion fuel was provided.

Comparison of catalytic effect on upgrading bio-oil derived from co-pyrolysis of water hyacinth and scrap tire over multilamellar MFI nanosheets and HZSM-5.

Catalytic co-pyrolysis of water hyacinth and scrap tire experiments were performed to evaluate the feasibility of improving the monocyclic aromatic hydrocarbons production. The production of monocyclic aromatic hydrocarbons increased from 5.31% (sole pyrolysis of water hyacinth) to 13.11% (co-pyrolysis with scrap tire). With use of zeolites, the highest production of monocyclic aromatic hydrocarbons can reach up to 69.18%. Comprehensive comparison on catalytic effects of HZSM-5 and multilamellar MFI nanosheets were provided. With the material to multilamellar MFI nanosheets ratios changes from 2:1 to 1:4, the production of monocyclic aromatic hydrocarbons increases significantly from 37.15-69.18%. The average production of monocyclic aromatic hydrocarbons produced by using multilamellar MFI nanosheets were 12.07% higher than that using HZSM-5, indicating the better performance of multilamellar MFI nanosheets in producing monocyclic aromatic hydrocarbons. This work provided a reference for the reuse of water hyacinth and scrap tire over multilamellar MFI nanosheets in energy field.