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Using diffusion kurtosis imaging (DKI) to evaluate the brain changes, the therapeutic effect and mechanism of tetramethylpyrazine in rats with dementia induced by lipopolysaccharide. Thirty-six male Sprague–Dawley rats were randomly divided into control group and five groups pretreated with sham operation, lipopolysaccharide(150ug) and three doses of tetramethylpyrazine(5, 10, and 20 mg/mL respectively). The Morris water maze test was used to evaluate cognitive ability. DKI and histology were performed. Low-dose of tetramethylpyrazine pretreated rats showed lower escape latency(6th day: 15.92seconds(s) vs. 5.11 s, P = 0.001), spent more time in the target quadrant(15.67 s vs. 29.83 s, P = 0.009) and crossed the platform area more frequently(3.50 vs. 9.17, P = 0.001) than rats in the LPS-treated group. Compared to sham group, the fractional anisotropy (FA), axial diffusion (Da), mean kurtosis (MK), and axial kurtosis (Ka) values in the cortex of lipopolysaccharide group were lower (P = 0.021,0.003,0.003,0.001,respectively).The MK, Ka, Kr, and FA values in the hippocampus of the lipopolysaccharide group were higher (P = 0.01, 0.026,0.007,0.003,respectively),while MD and Da values were lower (P = 0.045,0.044, respectively). Tetramethylpyrazine-pretreated rats showed higher values of FA, MD, Da, MK, and Ka in the cortex, lower MK, Ka, Kr, and FA values and higher MD,Da values in the hippocampus than the lipopolysaccharide group. Histologically, prominent inflammatory cells infiltration in the brain parenchyma of lipopolysaccharide group were observed, while groups pretreated using tetramethylpyrazine were alleviated. Tetramethylpyrazine can improve cognitive dysfunction induced by lipopolysaccharide. DKI can sensitively detect microstructure integrity of brain parenchyma in a non-invasive manner.

Combined antiretroviral therapy (cART) has significantly increased the life expectancy of AIDS patients; however, the prevalence of the neurocognitive impairment associated with HIV-1 continues to rise. HIV-1 gp120, an important subunit of the envelope spikes that decorate the surface of virions, is found to activate microglia in central nervous system (CNS) which leads to the cognitive and behavioral dysfunction known as HIV-1 associated neurocognitive disorder(HAND), and the V3 loop is the most important toxic domain of gp120. A study has shown that autophagy plays key role in the activation of microglia, p62 is an important autophagy substrate protein that is elevated in neuroinflammation. In this study, we sought to explore the role of p62 in gp120 V3 loop-mediated microglial activation. Our results demonstrated that exposure of CHME-5 cells to the gp120 V3 loop resulted in elevated inflammatory cytokines, accompanied by autophagy dysfunction and p62 upregulation. Subsequently, we found that the p62-dependent Nrf2 noncanonical signaling pathway was activated and that HO-1, the target protein of Nrf2, was also upregulated. Interestingly, the elevation of inflammatory factors caused by the gp120 V3 loop was significantly alleviated after knocking down p62, Nrf2 and HO-1. Further investigation revealed that in the microglial inflammation induced by the gp120 V3 loop, up-regulated HO-1 promoted the expression of iNOS by interacting with iNOS, while enhanced autophagy by RAPA promoted the degradation of iNOS and alleviated inflammation. These findings provide a new perspective on the relationship between noncanonical Nrf2 activation and autophagy in microglial inflammation and an experimental basis for HAND prevention and treatment.