RESUMO
Objectives: Gastrodia elata (GE) Blume (Orchidaceae) has been previously known for its therapeutic benefits against neurodegenerative diseases. Microglial activation and death have been implicated in the pathogenesis of a variety of neurodegenerative diseases, including Alzheimer's disease. In this study, GE and its pure components, gastrodin and 4-hydroxybenzyl alcohol (4HBA), were applied to β-amyloid-induced BV2 mouse microglial cells. Materials and Methods Cell viability was assessed by the MTT assay and Western blotting was also performed. Results: β-amyloid-induced cell death was shown to be induced time- and dose-dependently. To examine the cell death mechanism, we confirmed the involvement of ER stress signaling. C/EBP homologous protein (CHOP), a pro-apoptotic ER stress protein, was expressed at high levels but glucose-regulated protein 78 (GRP78), an anti-apoptotic ER stress protein with chaperone activity, was only slightly affected by treatment with β-amyloid. However, pretreatment with GE and its components inhibited the expression of CHOP but increased that of GRP78 in β-amyloid-treated cells. This study also showed that a single treatment with GE extracts, gastrodin, or 4HBA induced the expression of GRP78, a marker for enhanced protein folding machinery, suggesting a protective mechanism for GE against β-amyloid. Conclusions: This study reveals the protective effects of GE against β-amyloid-induced cell death, possibly through the enhancement of protein folding machinery of a representative protein, GRP78, and the regulation of CHOP in BV2 mouse microglial cells.
Assuntos
Animais , Camundongos , Amiloide/farmacologia , Álcoois Benzílicos/farmacologia , Morte Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Gastrodia/química , Glucosídeos/farmacologia , Microglia/efeitos dos fármacos , Álcoois Benzílicos/isolamento & purificação , Glucosídeos/isolamento & purificaçãoRESUMO
BACKGROUNDS/AIMS: To investigate the prevalence and clinical implications of hepatitis G virus (HGV) infection in patients with chronic renal failure, a cross-sectional study of 131 hemodialysis patients and 33 kidney transplantation recipients was conducted. METHODS: HGV RNA was amplified by reverse-transcription (RT) polymerase chain reaction (PCR) assay with primers from the 5'-untranslated region of the viral genome. RESULTS: The prevalence of HGV infection in patients with chronic renal failure was 25%(41/164). The following factors were taken into consideration: the mean age(43.15+/-11.97 years vs 46.46+/-13.08 years), the male to female ratio(2.15:1 vs 1.86:1), the mean of the dialysis duration(4.58+/-3.18 years vs 3.90+/-3.31 years), transfusion history (75.6% vs 62.6%), the mean of the ALT level during the prior 6 months(25.78+/-21.50 IU/L vs 23.00+/-59.49 IU/L), and the amount of transfusion(6.22+/-8.03 units vs 5.74+/-9.44 units). The anti-HCV(4.88% vs 8.94%) showed no difference between HGV RNA positive and negative group. The HBsAg positive ratio was 19.5% and 5.81% in HGV RNA positive group and negative group, respectively. CONCLUSION: The prevalence of HGV infection in patients with chronic renal failure was 25%. There was a higher rate of HBsAg positivity in the HGV RNA positive group rather than in the negative group. HGV infection did not seem to be associated with clinically significant hepatitis.