Objective:To investigate the effects of anxiety and depressive symptoms in mediation of pain catastrophizing on disability in patients with low back pain.Methods:A cross-sectional survey was conducted among 97 patients with low back pain in the Changjiang Subdistrict community health center from July to October 2021. Oswestry Disability Index, pain catastrophic subscale in Coping Strategies Questionnaire-24, Generalized Anxiety Disorder Scale-short version, Patient Health Depression Questionnaire-short version were used to evaluate the activity dysfunction, pain catastrophic cognition and anxiety and depression levels of patients,respectively. Path analysis was implemented to test the mediation model, and the indirect effects were assessed using the bootstrap procedure with bias-corrected 95 %CI. Results:Results suggested significant positive correlations among pain catastrophizing, anxiety, depressive symptoms and disability of patients. In addition, both anxiety and depressive symptoms significantly mediated the impact of pain catastrophizing on disability (standardized indirect effects were 0.183 and 0.197, P<0.05). Patients with higher levels of pain catastrophic cognition showed higher levels of anxiety and depressive symptoms (β=0.757, 0.720; P<0.01), and reported more severe motor dysfunction (β=0.241, 0.274; P<0.05). Conclusions:Our findings suggest that anxiety and depression may be the psychological pathways through which pain catastrophizing predicts disability in patients with low back pain. Effective psychological interventions, such as emotion regulation and stress reduction strategies should be considered in treatment and supportive care for patients with low back pain.

Polygonum multiflorum （PM）， a commonly used Chinese herbal medicine in clinical practice， has been associated with frequent reports of liver injury in recent years， and the medication safety of PM has attracted more and more attention in China and globally. This article reviews the recent research advances in the signaling pathways and mechanisms of PM in causing drug-induced liver injury （DILI） and aims to provide new ideas for the proper and rational use of PM in clinical practice. The results show that PM is involved in the regulation of various signaling pathways， and it leads to the death of hepatocytes by destroying mitochondrial function， exacerbating bile acid accumulation， and inducing immune response， oxidative stress， and endoplasmic reticulum stress， thereby inducing the development and progression of DILI through multiple targets， pathways， and levels.