Evaluation of effect of horticultural therapy on improving mental health in university students / 中国学校卫生

Objective@#To investigate the effectiveness of horticultural therapy on improving university students mental health problems and to provide evidence to support the application of horticultural therapy in the prevention and treatment of university students mental health.@*Methods@#From March to May 2022,a before-and after paired design was used with a blank control group, mental health screening abnormalities were recruited from a comprehensive university in Hebei Province, including 57 in the intervention group and 21 in the control group, and the Symptom Checklist-90(SCL-90) score and hair cortisol were included as outcome indicators, which was measured by enzyme linked immunoassay Elisa double antibody sandwich method.@*Results@#The total SCL-90 scores of the intervention group decreased ( t=4.28, P <0.01) and were significantly lower compared with the control group( t=-2.66, P <0.01), while no significant difference was observed in the control group( t=0.29, P >0.05), and the difference between the pre and post measures on each dimension of the SCL-90 was significantly lower in the intervention group (all P <0.01); the difference between the pre and post measures of hair cortisol contentration in the intervention group was statistically significant( Z= -2.75, P <0.05), and the hair cortiso contentration in pre measure group was lower than that of control group( Z=-3.48, P < 0.01 ). In contrast, the difference between pre and post measurements of hair cortisol in the control group was not significant( Z= -0.75 , P >0.05).@*Conclusion@#Horticultural therapy can improve the psychological symptoms of university students is suitable for psychological interventions in the university population and is beneficial to the health and well being of university students.

Low-dose paclitaxel modulates the cross talk between the JNK and Smad signaling in primary biliary fibroblasts

SUMMARY OBJECTIVE: The objective of this study was to explore the molecular mechanism underlying the occurrence of benign bile duct stricture and the target of low-dose paclitaxel in the prevention of benign bile duct stricture. METHODS: Under the stimulation of transforming growth factor beta 1, the expression of collagen type I and connective tissue growth factor were detected on isolated primary fibroblasts. The phosphorylation levels of JNK and Smad2L were detected using Western blot. The effect of low-dose paclitaxel on the transforming growth factor beta 1-induced inhibition of type I collagen and connective tissue growth factor expression and JNK and Smad2L phosphorylation was also observed. RESULTS: Transforming growth factor beta 1 induced the secretion of type I collagen and connective tissue growth factor as well as JNK phosphorylation in biliary fibroblasts. The JNK inhibitor or siRNA-Smad2 inhibited the transforming growth factor beta 1-induced secretion of type I collagen and connective tissue growth factor. Low-dose paclitaxel inhibited the expression of type I collagen induced by transforming growth factor beta 1 and may inhibit the secretion of collagen in biliary fibroblasts. CONCLUSION: The activation of JNK/Smad2L induced by transforming growth factor beta 1 is involved in the occurrence of benign bile duct stricture that is mediated by the overexpression of type I collagen and connective tissue growth factor, and low-dose paclitaxel may inhibit the phosphorylation of JNK/Smad2L.

Platelet-derived growth factor mediates interleukin-13-induced collagen I production in mouse airway fibroblasts.

Interleukin-13 (IL-13) is associated with the production of collagen in airway remodelling of asthma. Yet, the molecular mechanisms underlying IL-13 induction of collagen remain unclear; the aim of this study is to address this issue. IL-13 dose- and time-dependently-induced collagen I production in primary cultured airway fibroblasts; this was accompanied with the STAT6 phosphorylation, and pre-treatment of cells with JAK inhibitor suppressed IL-13- induced collagen I production. Further study indicated that IL-13 stimulated JAK/STAT6-dependent PDGF production and subsequent ERK1/2 MAPK activation in airway fibroblasts, and the presence of either PDGF receptor blocker or MEK inhibitor partially suppressed IL-13-induced collagen I production. Taken together, our study suggests that activation of JAK/STAT6 signal pathway and subsequent PDGF generation and resultant ERK1/2 MAPK activation mediated IL-13-induced collagen I production in airway fibroblasts.