ABSTRACT
BACKGROUND: G protein coupled receptor kinase 2 (GRK2) has been demonstrated to play a crucial role in the development of chronic pain. Acupuncture is an alternative therapy widely used for pain management. In this study, we investigated the role of spinal neuronal GRK2 in electroacupuncture (EA) analgesia. METHODS: The mice model of inflammatory pain was built by subcutaneous injection of Complete Freund's Adjuvant (CFA) into the plantar surface of the hind paws. The mechanical allodynia of mice was examined by von Frey test. The mice were subjected to EA treatment (BL60 and ST36 acupuncture points) for 1 week. Overexpression and down-regulation of spinal neuronal GRK2 were achieved by intraspinal injection of adeno associated virus (AAV) containing neuron-specific promoters, and microglial activation and neuroinflammation were evaluated by real-time PCR. RESULTS: Intraplantar injection with CFA in mice induced the decrease of GRK2 and microglial activation along with neuroinflammation in spinal cord. EA treatment increased the spinal GRK2, reduced neuroinflammation, and significantly decreased CFA-induced mechanical allodynia. The effects of EA were markedly weakened by non-cell-specific downregulation of spinal GRK2. Further, intraspinal injection of AAV containing neuron-specific promoters specifically downregulated neuronal GRK2, and weakened the regulatory effect of EA on CFA-induced mechanical allodynia and microglial activation. Meanwhile, overexpression of spinal neuronal GRK2 decreased mechanical allodynia. All these indicated that the neuronal GRK2 mediated microglial activation and neuroinflammation, and subsequently contributed to CFA-induced inflammatory pain. CONCLUSION: The restoration of the spinal GRK2 and subsequent suppression of microglial activation and neuroinflammation might be an important mechanism for EA analgesia. Our findings further suggested that the spinal GRK2, especially neuronal GRK2, might be the potential target for EA analgesia and pain management, and we provided a new experimental basis for the EA treatment of pain.
Subject(s)
Animals , Mice , Electroacupuncture , Microglia/physiology , G-Protein-Coupled Receptor Kinase 2/physiology , Pain Management , Pain/chemically induced , Inflammation/chemically induced , Inflammation/therapy , NeuronsABSTRACT
AIM:To compare the retinal nerve fiber layer (RNFL) thickness in patients with different severities of obstructive sleep apnea-hypopnea syndrome (OSAHS) versus normal controls.METHODS:This was an observational case-control study.Totally 79 patients presenting with snoring and daytime sleepiness who underwent overnight polysomnography (PSG) to determine OSAHS severity were recruited,and subsequently referred for ophthalmologic evaluation.The data including intraocular pressure (lOP),RNFL thickness etc was collected.RESULTS:A total of 73 subjects were recruited,including 53 patients with OSAHS and 20 normal control subjects.lOP was significantly higher for the moderate and severe OSAHS group than for the control group (both P＜0.05).The RNFL in the average and superior quadrants were significantly thinner for the moderate and severe OSAHS group than for the control group (both P＜0.05).AHI was negatively correlated with RNFL thickness in the superior quadrants,and with average RNFL thickness (r=-0.316,-0.205;both P＜0.01).Negative correlations were also identified between RNFL thickness in the superior quadrants and the ODI (r=-0.24,P =0.005).Positive correlations were identified between SaO2 on PSG and RNFL thickness in the superior quadrants (r=0.277,P=0.001).CONCLUSION:RNFL of the patients with OSAHS is thinned.Furthermore,it is observed that the greater severity of OSAHS,the greater the loss of RNFL.Among the four quadrants observed,the most affected quadrant was the superior quadrant.
ABSTRACT
Congenital skeletal deformity of ferns varies and may be attributed to a range of reasons.Congenital skeletal deformity seriously affects body function or even leads to neonatal death directly.The disease brings great pain to victim and their family.We reviewed the fetal prenatal ultrasonic data conducted during period from Jan.2013 to June 2016,and there were 84 fetuses with skeletal abnormalities among 12 000 cases,and 3 fetuses with thanatophoric dysplasia.Our report described and reviewed three common types of thanatophoric dysplasia,aiming to explore the value of standardized prenatal ultrasonic diagnosis of fetal abnormalities in the skeletal system.
ABSTRACT
OBJECTIVES: The biological functions of transforming growth factor-β signaling that involves Smad proteins have not been previously investigated with respect to coronary artery bypass grafts. The aim of the present study was to observe the immunostaining of proteins that are related to this signaling pathway. METHODS: Fifteen remnants of coronary artery bypass grafts, including nine saphenous veins, three radial arteries and three mammary arteries, were collected from 12 patients who were undergoing coronary artery bypass. Hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining of transforming growth factor-β1, type I receptor of transforming growth factor-β, Smad2/3, Smad4, and Smad7 were performed. RESULTS: The saphenous veins showed more severe intimal degeneration, more severe smooth muscle cell proliferation and more collagen deposition than the arterial grafts, as evidenced by hematoxylin and eosin and Masson's trichrome stainings. Immunohistochemical assays demonstrated that the majority of the transforming growth factor-β1 signaling cytokines were primarily localized in the cytoplasm in the medial layers of all three types of grafts, whereas ectopic transforming growth factor-β1, type I receptor of transforming growth factor-β, and Smad7 overexpressions in the interstices were observed particularly in the saphenous vein and radial arterial grafts. CONCLUSION: Enhanced transforming growth factor-β1 signal transduction with medial smooth muscle cell proliferation and ectopic transforming growth factor-β1, the presence of the type I receptor of transforming growth factor-β, and Smad7 overexpressions in the extracellular matrix may provide primary evidence for early or late graft failure.