Puerarin protected rats with traumatic brain injury through autophagy regulation via JNK pathway

Abstract

Objective To explore the impact of puerarin treatment on autophagy in rats with traumatic brain injury (TBI) and the underlying mechanism. Methods Seventy five Sprague-Dawley (SD) rats were randomized into 5 groups: sham group (S group, n=15), traumatic brain injury group (TBI group, n=15), TBI+ puerarin treatment group (TBI+ Pue group, n=15), TBI+ JNK inhibitor group (TBI+ SP group, n=15), and TBI+ JNK activator+ Pue (TBI+ An+ Pue group, n=15). Feeney method was applied to make rats with TBI model. After that, head water content and neurological deficit score (NDS) were measured and recorded at day 1, 3 and 7 in each group. Western blot was used to measure the JNK activity and autophagic marker proteins, including LC3B and Beclin1. Results Compared to S group, the head water content and NDS were decreased significantly among the others (P<0.05). The head water content and NDS in TBI+ Pue and TBI+ SP groups was decreased remarkably compared with TBI group. Combined with puerarin and animycin treatments failed to reduce head water content and NDS compared to the TBI+ Pue group. Activated autophagy could be observed in TBI group compared to S group. Compared to group S, LC3II, Beclin1 and P-JNK1 were increased significantly. Pue and SP could reduce their expressions, respectively. Combined with puerarin and animycin treatments failed to reduce LC3II, Beclin1 and P-JNK1 compared to TBI+ Pue group. Conclusions Puerarin could protect rats with TBI via inhibiting autophagy, JNK signal pathway could involve the process of puerarin regulating autophagy. Key words: PUERARIN/PD; Brain injuries/DT/ME/PA; Autophagy/DE; JNK mitogen-activated protein kinases/ME/DE; Signal transduction/DE