The cholinergic anti-inflammatory pathway (CAIP) is important for antagonizing inflammation and treating several diseases, including acute respiratory distress syndrome (ARDS), and is related to vagus nerve integrity. However, its underlying pathophysiological mechanism is still unclear. We hypothesized that CAIP regulates lung injury repair after ARDS through the STAT3 signaling pathway, which is an important downstream effector of α7nAchR. We enhanced CAIP activity by subjecting rats to vagus nerve stimulation (VNS), and administered the α-7 acetylcholine receptor (α7nAchR) agonist and antagonist to determine whether VNS can reduce lung injury by regulating the pulmonary inflammatory response through CAIP. After being subjected to VNS, the secretion of TNF-α and IL-1β was decreased, while the level of IL-10 was increased in the rat model of ARDS. Moreover, VNS treatment reduced lung mRNA levels of M1 macrophage markers, while increased those of M2 macrophage markers. The expression of Caspase-1 decreased, while that of STAT3 increased in lung tissue after VNS treatment. The aforementioned effects of VNS were reversed by cutting the cervical vagus efferent branch and blocking α7nAchR. These findings suggest that VNS inhibits the ARDS inflammatory response by promoting CAIP activity. Next, we used lentivirus knockdown of STAT3 expression to explore the mechanism of VNS through CAIP on lung inflammation in ARDS model rats. VNS activates α7nAchR, increases STAT3 expression, reduces Caspase-1 expression, suppresses inflammation by inhibiting inflammatory pyroptosis and M1 to M2 macrophage transformation, which may constitute the main mechanism of VNS action in ARDS.
The therapeutic efficacy of J3N in treating GAD is equivalent to, but with the efficacy index significantly higher than, that of conventional treatment. Moreover, when combined with drugs, needling might effectively prevent the side effect of the routinely used Western drugs. The regulatory action of needling on platelet 5-HT and plasma ACTH is probably one of the acting pathways for J3N treatment on GAD.
Introduction:
Growing evidence indicates that testosterone is a conspicuous marker for assessing male bone mineral density (BMD). However, research regarding testosterone levels and BMD is sparse and controversial for females. Hence, we aimed to investigate the association between testosterone levels and BMD among adult females aged 40–60 years in America.
Methods
In this cross-sectional study, all individuals were part of the National Health and Nutrition Examination Survey (2011–2016). A weighted general linear model was used to estimate the association between testosterone and lumbar BMD. Age, race, income level, education level, body mass index (BMI), blood urea nitrogen (BUN) level, serum uric acid (UA) level, serum calcium (Ca) level, serum phosphorus (P) level, oral contraceptive use, female hormones use(estrogen and progesterone), smoking status, drinking status were adjusted using a weighted multiple regression model.
Results
We included 2198 female individuals in the study, testosterone levels were positively associated with lumbar BMD after adjusting for all the covariates (β = 0.0008, 95% confidence interval = 0.0001, 0.0015, P < 0.05). Subgroup analysis showed that the results remained stable.
Conclusions
In US adults female aged 40–60 years, the testosterone level was an independent positive correlation with the lumbar BMD after adjusting for covariates. Based on our findings, testosterone may be a marker for predicting osteoporosis in females.
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