BACKGROUND:Macrophages exhibit distinct pro-inflammatory and anti-inflammatory phenotypes.Through tissue engineering techniques,their phenotype transition has made them one of the most studied immune cells in bone injury repair.Recent studies have found that neutrophils also play a significant role in bone injury repair processes,but there is currently no such review available.OBJECTIVE:To summarize the current role of neutrophils in fracture healing and interventions targeting neutrophils to promote fracture healing.METHODS:We searched the Web of Science,PubMed,WanFang Data,and CNKI databases from January 2000 to February 2024 with the key words of"neutrophil,fracture healing,bone damage,bone repair,bone remodeling"in Chinese and English.Literature screening was conducted based on inclusion and exclusion criteria,resulting in a final selection of 72 articles for review.RESULTS AND CONCLUSION:(1)The history of neutrophils has been long,with their importance initially overlooked due to a lack of staining techniques.In 1900,Paul Ehrlich's invention of triacid staining distinguished neutrophils,marking the beginning of research in this field.(2)Under normal conditions,neutrophils migrate to various organs to assist in their physiological functions.In pathological states,neutrophils exert their antimicrobial effects through phagocytosis,degranulation,and the formation of neutrophil extracellular traps.(3)Neutrophils primarily participate in the early hematoma inflammation stage of fracture healing by releasing cytokines to recruit other immune cells and mesenchymal stem cells.They also produce fibrinogen to promote hematoma formation and establish a local microenvironment.(4)Neutrophils transform into two distinct subtypes,N1 and N2,at different stages of fracture healing,coordinating with each other to promote bone repair.(5)Neutrophils recruited to the fracture site participate in the healing process by secreting cytokines such as tumor necrosis factor-alpha,interleukin-6,interleukin-10,fibroblast growth factor-2,monocyte chemoattractant protein-1,and platelet-derived growth factor.(6)Neutrophils regulate osteogenesis/osteolysis balance through interactions with the main cellular components involved in different stages of fracture healing.(7)Similar to the widespread research and application of tissue engineering techniques in modulating macrophage polarization in fracture healing,interventions targeting neutrophils to promote fracture healing hold promising prospects for the future.

OBJECTIVE: To observe the clinical effect of acupuncture-moxibustion therapy of Daoqi Tongluo (conducting qi and unblocking collateral) on chronic primary tinnitus. METHODS: A total of 32 patients with chronic primary tinnitus were included and treated with the acupuncture-moxibustion therapy of Daoqi Tongluo. This regimen was composed of abdominal acupuncture, body acupuncture, warm needling and posterior-auricular local flashing cupping, Zhongwan (CV12), Guanyuan (CV6) and Yindu (KI9), Tinggong (SI19), Cong'er point, Waiguan (TE5) of the affected side, etc. are selected. The treatment was given once every two days, 3 treatments a week; and one course of intervention was required, with 10 treatments included. Before and after treatment, the scores of tinnitus handicap inventory (THI), tinnitus evaluation questionnaire (TEQ), self-rating scale of sleep (SRSS), self-rating anxiety scale (SAS), and self-rating depression scale (SDS) were observed, and the clinical effect was evaluated. RESULTS: After interventions, the scores of THI, TEQ, SRSS, SAS and SDS were reduced in comparison with those before interventions in the patients (P<0.001, P<0.01, P<0.05), and the total effective rate was 71.9% (23/32). CONCLUSION Acupuncture-moxibustion therapy of Daoqi Tongluo is effective on chronic primary tinnitus and this therapy can alleviate tinnitus degree, improve sleep quality and attenuate the anxious and depressive emotion of the patients.
Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Young Adult ; Acupuncture Points ; Acupuncture Therapy ; Chronic Disease/therapy* ; Moxibustion ; Tinnitus/psychology* ; Treatment Outcome

BACKGROUND:Macrophages exhibit distinct pro-inflammatory and anti-inflammatory phenotypes.Through tissue engineering techniques,their phenotype transition has made them one of the most studied immune cells in bone injury repair.Recent studies have found that neutrophils also play a significant role in bone injury repair processes,but there is currently no such review available.OBJECTIVE:To summarize the current role of neutrophils in fracture healing and interventions targeting neutrophils to promote fracture healing.METHODS:We searched the Web of Science,PubMed,WanFang Data,and CNKI databases from January 2000 to February 2024 with the key words of"neutrophil,fracture healing,bone damage,bone repair,bone remodeling"in Chinese and English.Literature screening was conducted based on inclusion and exclusion criteria,resulting in a final selection of 72 articles for review.RESULTS AND CONCLUSION:(1)The history of neutrophils has been long,with their importance initially overlooked due to a lack of staining techniques.In 1900,Paul Ehrlich's invention of triacid staining distinguished neutrophils,marking the beginning of research in this field.(2)Under normal conditions,neutrophils migrate to various organs to assist in their physiological functions.In pathological states,neutrophils exert their antimicrobial effects through phagocytosis,degranulation,and the formation of neutrophil extracellular traps.(3)Neutrophils primarily participate in the early hematoma inflammation stage of fracture healing by releasing cytokines to recruit other immune cells and mesenchymal stem cells.They also produce fibrinogen to promote hematoma formation and establish a local microenvironment.(4)Neutrophils transform into two distinct subtypes,N1 and N2,at different stages of fracture healing,coordinating with each other to promote bone repair.(5)Neutrophils recruited to the fracture site participate in the healing process by secreting cytokines such as tumor necrosis factor-alpha,interleukin-6,interleukin-10,fibroblast growth factor-2,monocyte chemoattractant protein-1,and platelet-derived growth factor.(6)Neutrophils regulate osteogenesis/osteolysis balance through interactions with the main cellular components involved in different stages of fracture healing.(7)Similar to the widespread research and application of tissue engineering techniques in modulating macrophage polarization in fracture healing,interventions targeting neutrophils to promote fracture healing hold promising prospects for the future.

Objective To investigate the neuroprotective effect of methylene blue on diabetic retinopathy in rats. Methods Thirty SD rats were randomly divided into blank, control and experimental groups. The control and experimental groups were induced with diabetes by streptozotocin (STZ) intraperitoneal injection. After 6 weeks of successful modeling, the experimental group received intravitreal injection of methylene blue at a dose of [0.2 mg/(kg.d)], while the control group received an equal amount of dimethyl sulfoxide (DMSO) intravitreal injection, both continuously injected for 7 days. ELISA was used to detect the levels of retinal superoxide dismutase (SOD), 8-iso-prostaglandin F2alpha (iPF2α) and interleukin-1β (IL-1β) in rats. Western blot analysis was used to detect the expression of retinal extracellular signal-regulated kinase 1/2 phosphorylation (p-ERK1/2) and phosphorylated protein kinase B (p-AKT), and PAS staining was used to detect retinal morphological changes. Results Compared with the blank group rats, the retinal SOD activity in the control and experimental group rats was significantly reduced. iPF2α, IL-1β and p-ERK1/2 level increased, while p-AKT level decreased. Compared with the control group, the SOD activity of the experimental group rats increased. iPF2α and IL-1β level went down, while p-ERK1/2 and p-AKT level went up significantly. The overall thickness of the retinal layer and the number of retinal ganglion cells were significantly reduced. Conclusion Methylene blue improves diabetic retinopathy in rats by reducing retinal oxidative stress and enhancing ERK1/2 and AKT phosphorylation.
Rats ; Animals ; Diabetic Retinopathy/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism* ; Mitogen-Activated Protein Kinase 3/metabolism* ; Interleukin-1beta/metabolism* ; Methylene Blue/pharmacology* ; Phosphorylation ; Rats, Sprague-Dawley ; MAP Kinase Signaling System ; Diabetes Mellitus, Experimental/drug therapy* ; Superoxide Dismutase/metabolism*

Objective: To investigate the effect of peroxide reductase 1 (Prdx1) on myocardial hypertrophy and fibrosis in spontaneously hypertensive rats，and to analyze its mechanism． Methods: Forty five SHR rats were randomly divided into model group (SHR group) ，AAV9-NC group and AAV9-Prdx1 group．There were 15 WKY rats in each group，and the other 15 Wistar Kyoto rats were set as the control group．The rats in each group were administered continuously for 8 weeks，and the indexes of cardiac function were detected by echocardiography ; The mean blood pressure and myocardial hypertrophy were measured ; HE staining and Masson staining were used to observe the histomorphology and fibrosis of rat myocardium ; The indexes of oxidative stress in rat serum were detected by ELISA ; The expression level of Prdx1 mRNA in rat myocardium was detected by qRT-PCR ; Western blot was used to detect the expression of Prdx1 protein and nuclear factor E2 related factor 2 (Nrf2) / heme oxygenase-1 (HO-1) signaling pathway related proteins in rat myocardium. Results: Compared with the Control group，the expression of Prdx1 mRNA and protein ，left ventricular ejection fraction ( EF) and left ventricular shortening rate ( FS) decreased in SHR group (P＜0. 05) ，the mean blood pressure，heart mass index ( HMI) and left ventricular mass index (LVMI) of rats increased (P＜0. 05) ，and there were obvious pathological damage and collagen fiber deposition in myocardial tissue．The activities of superoxide dismutase (SOD) and glutathione peroxidase ( GSH-Px) in rat serum decreased，and the content of malondialdehyde (MDA) increased (P＜0. 05) ; The expression of Nrf2， HO-1 and quinone oxidoreductase 1 (NQO1) protein decreased in myocardial tissue (P＜0. 05) ．Compared with SHR group，the expression of Prdx1 mRNA and protein，EF and FS in myocardial tissue of AAV9-Prdx1 group increased (P＜0. 05) ，the mean blood pressure，HMI and LVMI of rats decreased (P＜0. 05) ，and myocardial tissue injury and myocardial fibrosis improved ; The activities of SOD and GSH-Px in rat serum increased，while the content of MDA decreased (P＜0. 05) ; The expression of Nrf2，HO-1 and NQO1 protein increased in myocardial tissue (P＜0. 05) ． Conclusion Overexpression of Prdx1 can reduce myocardial hypertrophy and fibrosis and improve cardiac function in SHR rats．Its mechanism may be related to activating Nrf2 / HO-1 signaling pathway and inhibiting oxidative stress response.