Abstract: BACKGROUND: Crush injury syndrome often causes substantial organ damage, and the disease progresses rapidly with a high mortality. To explore its pathological mechanism can relieve ischemia-reperfusion injury, and thereby improve the pathological symptoms of crush injury.
OBJECTIVE: To study the effects of Mailuoning Injection on mitochondrial autophagy and PINK1/Parkin pathway in the crush injury syndrome model pigs. 
METHODS: Bama miniature pigs were randomly divided into four groups: control group, model group, perfusion group, and Mailuoning group. A crush injury model was prepared in all groups except for the control group. The perfusion group was subjected to cardiopulmonary bypass with 50 mL of saline at a speed of 50 mL/h first and then restoring autologous blood supply. The Mailuoning group was subjected to cardiopulmonary bypass with 50 mL of Mailuoning injection at a speed of 50 mL/h. The model group was not treated. Six hours after the recovery of autogenous blood supply, the biochemical indexes, including creatinine, urea nitrogen, creatine kinase, alanine aminotransferase, aspartate aminotransferase, and potassium ion, were measured by automatic biochemical analyzer. The levels of serum interleukin-1β, interleukin-6 and tumor necrosis factor α were detected by ELISA. Hematoxylin-eosin staining was used to observe the pathological changes of tibialis anterior muscle tissues; the changes of mitochondria and autophagosomes were observed by transmission electron microscopy. Western blot was used to detect the expression of microtubule associated protein 1 light chain 3 (LC3)-I and II, PINK1 and Parkin proteins. 
RESULTS AND CONCLUSION: Compared with the control group, in the model group and perfusion group, the myofilaments of tibialis anterior muscle tissues were disordered and inflammatory cells infiltrated, the levels of creatinine, urea nitrogen, creatine kinase, alanine aminotransferase, aspartate aminotransferase, potassium ion, interleukin-1β, interleukin-6 and tumor necrosis factor α in serum were significantly higher (P < 0.001), the number of autophagosomes and the expressions of LC3-II/LC3-I, PINK1 and Parkin proteins in tibialis anterior muscle tissues were significantly lower (P < 0.05). Compared with the model group and the perfusion group, the above pathological symptoms of tibialis anterior muscle tissues were significantly reduced in the Mailuoning group, the levels of serum biochemical indexes and inflammatory indexes were significantly lower (P < 0.001), and the number of autophagosomes and the expressions of LC3-II/LC3-I, PINK1 and Parkin proteins in tibialis anterior muscle tissues were significantly higher (P < 0.05). To conclude, Mailuoning Injection may activate mitochondrial autophagy through PINK1/Parkin pathway and improve the pathological symptoms of crush injury.

Key words: Mailuoning Injection, crush injury syndrome, cardiopulmonary bypass perfusion, tibialis anterior muscle, mitochondria, authophagy, pathway