Objective: To analyze the occurrence and risk factors of various occupational hazard incidents in China's power grid enterprises. Methods: A total of 4 191 workers from eight power grid enterprises in Jilin Province, Shandong Province, and Chongqing City were selected using a convenience sampling method. Their exposure in workplace and the occurrence of various occupational hazard incidents from 2018 to 2020 were investigated. Results: Among the participants, 71.7% were engaged in outdoor operations. The incidence rates of occupational hazard emergency, ranking from high to low, were electric ophthalmia, acute mountain sickness, heatstroke, electro-flash dermatitis, sunburn, cold injury, solar ophthalmia, and gas poisoning in confined space, with the rate of 42.3%, 42.3%, 38.1%, 24.3%, 17.4%, 16.5%, 10.0%, and 1.3%, respectively (P<0.01). The results of multivariate logistic regression analysis showed that workers in Jilin Province had a higher risk of cold injury compared to those in Shandong Province and Chongqing City (all P<0.01). Workers in Chongqing City had a higher risk of solar ophthalmia than those in Jilin Province (P<0.01). Workers in inspection and maintenance positions had a higher risk of heatstroke and sunburn compared to those in substation positions (all P<0.05). Power grid workers with protective systems in enterprises had a lower risk of sunburn and solar ophthalmia compared to those without protective systems (all P<0.01). The risks of sunburn and solar ophthalmia among power grid workers increased with age and daily outdoor working time (all P<0.05). Taking protective measures was a protective factor against heatstroke and cold injury (all P<0.01). Conclusion: Power grid workers face the risk of various occupational hazard incidents. Relevant organizations should conduct targeted preventive measures based on regional and worker characteristics, and ensure the implementation of protective systems in different work environments.

Chuanxiong Rhizoma (CX, the dried rhizome of Ligusticum wallichii Franch.), a well-known traditional Chinese medicine, is clinically used for treating cardiovascular, cerebrovascular and hepatobiliary diseases. Cholestatic liver damage is one of the chronic liver diseases with limited effective therapeutic strategies. Currently, little is known about the mechanism links between CX-induced anti-cholestatic action and intercellular communication between cholangiocytes and hepatic stellate cells (HSCs). The study aimed to evaluate the hepatoprotective activity of different CX extracts including the aqueous, alkaloid, phenolic acid and phthalide extracts of CX (CX_AE, CX_AL, CX_PA and CX_PHL) and investigate the intercellular communication-related mechanisms by which the most effective extracts work on cholestatic liver injury. The active compounds of different CX extracts were identified by UPLC-MS/MS. A cholestatic liver injury mouse model induced by bile duct ligation (BDL), and transforming growth factor-β (TGF-β)-treated human intrahepatic biliary epithelial cholangiocytes (HIBECs) and HSC cell line (LX-2 cells) were used for in vivo and in vitro studies. Histological and other biological techniques were also applied. The results indicated that CX_AE, CX_AL and CX_PHL significantly reduced ductular reaction (DR) and improved liver fibrosis in the BDL mice. Meanwhile, both CX_AE and CX_PHL suppressed DR in injured HIBECs and reduced collagen contraction force and the expression of fibrosis biomarkers in LX-2 cells treated with TGF-β. CX_PHL suppressed the transcription and transfer of plasminogen activator inhibitor-1 (PAI-1) and fibronectin (FN) from the 'DR-like' cholangiocytes to activated HSCs. Mechanistically, the inhibition of PAI-1 and FN by CX_PHL was attributed to the untight combination of the acetyltransferase KAT2A and SMAD3, followdd by the suppression of histone 3 lysine 9 acetylation (H3K9ac)-mediated transcription in cholangiocytes. In conclusion, CX_PHL exerts stronger anti-cholestatic activity in vivo and in vitro than other CX extracts, and its protective effect on the intracellular communication between cholangiocytes and HSCs is achieved by reducing KAT2A/H3K9ac-mediated transcription and release of PAI-1 and FN.