ABSTRACT
AIM: To investigate the effects of curcumin (Cur) on the expression of High mobility group box 1 protein (HMGB1), interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α) in amyloid-β(Aβ)-induced primary rat microglial cells.METHODS: Microglia were derived from the cerebral cortices of postnatal rat brains.The cells were i-dentified by immunocytochemistry using mouse anti rat Iba-1 monoclonal antibody.A cell model using primary rat microgli-al cells incubated with Aβ25-35 as an inflammation model of Alzheimer’s disease (AD) was set up.The morphological char-acters of primary rat microglial cells were observed.The concentration of Aβ25-35 and the treatment concentration of curcumin were selected by CCK-8 assay.Cultured primary rat microglial cells were divided into 5 groups: normal cell group, Aβ25-35 group, Cur group, Aβ25-35 +Cur group and Aβ25-35 +DMSO group.The expression of HMGB1, NF-κB, and receptor for advanced glycation end products (RAGE) was detected by Western blot.The levels of HMGB1, IL-1β, and TNF-αin the culture supernatant were measured by ELISA.RESULTS: The purity of primary microglias determined by Iba-1 immuno-fluorescence was more than 95%.The protein levels of HMGB1, RAGE and NF-κB were significantly increased after Aβ25-35 stimulation.After treatment with Cur, the protein levels of HMGB1, RAGE and NF-κB were significantly decreased (P <0.05).The levels of HMGB1, IL-1βand TNF-αin the supernatant were significantly increased after Aβ25-35 stimula-tion.Cur significantly decreased the level of HMGB1, IL-1βand TNF-αin the supernatant.CONCLUSION: Curcumin significantly inhibits neuroinflammation stimulated by Aβ25-35 in primary rat microglial cells.
ABSTRACT
Objective To demonstrate the spectrum of multi-detector spiral CT (MSCT) findings of drug-induced liver injury (DILI). Methods From May 2008 to January 2010, DILI was identified in 10 cases based on their clinical and pathological results. The spectrum of CT findings was analyzed retrospectively. Results According to the CT features, DILI were divided into three types. ( 1 ) Two cases presented diffuse hepatic injury, which appeared as homogeneous hypo-attenuation in precontrast CT scan and mild enhancement after contrast injection. The histopathological findings of the involved 1ivers include hepatocellular steatosis, neutrophil and eosinophil infiltration, punctiform necrosis and canalicular cholestasis. (2) Six cases presented focal hepatic injury, including massive wedge-shaped necrosis in 4,multiple small necroses in 1 and multiple regenerated nodules in 1. In precontrast CT scan, hepatic necroses were seen as inhomogeneous hypo-attenuation areas, which turned to hyper-attenuation after contrast injection and presented "flip-flop" sign between precontrast CT scan and portal venous phase scan. In the case with regenerated nodules, slight hyper-attenuation lesions were detected with diffuse distribution in liver in precontrast CT scan, which showed enhancement in hepatic arterial phase and turned to iso-attenuation in portal venous phase and equilibrium phase. The histopathological changes included massive necrosis or bridging necrosis with abundant neutrophil and eosinophil infiltration in 5 cases, nodular regeneration with cholestasis and feathery degeneratin in 1 case. (3) Two cases presented liver cirrhosis. CT displayed obvious nodularity of liver, which complicated with splenomegaly, ascites and collateral veins. The histopathological changes of these two cases included punctiform necrosis, canalicular cholestasis and pseudolobular formation. Conclusion CT signs of DILl have certain characteristics, which may help in detecting and determining the severity of liver damage.