Abstract

Objective To observe the effect of aqueous extract of Broussonetia papyrifera ( L. ) Vent on the ability of space learning and memory in the rats with Alzheimer' s disease (AD) induced by Aβ 25-35 and Dgalactose and to explore the mechanisms underlying those improvements. Methods The animal model of AD was established by Aβ 25-35 stereotactic injection into the hippocampus of rats in 5 minutes,while long-term intraperitoneal injection with D-gal. After the injection of Aβ25-35,rats were treated with aqueous extract of Broussonetia papyrifera ( L. ) Vent for the next 30 days. Morris water maze with computer system and the spatial exploration experiments were used to assess the behavior performances of the rats. Immunohistochemical technique was used to detect the expression of BiP, PERK and CHOP. Results The ability of space learning and memory of rats complex model of Alzheimer's disease induced by Aβ25-35 and D-gal was damaged,while escape latency was (20.90± 9.16 ) s,and the proportion of original platform quadrant was ( 11.05 ± 4.43 ) %. The expression level of Bip was reduced ,while the mean gray was ( 139.71 ± 3.47 ). The expression level of PERK and CHOP was increased,while the mean gray were (97.96 ± 5.97 ), ( 110.93±4.91 )separately. The escape latency of rats in the aqueous extract of Broussonetia papyrifera ( L. ) Vent treated groups was ( 5.41 ± 3.47 ) s and shorter than the model group,while the proportion of original platform quadrant was (48.28 ± 7.03 )% and higher than the model group.The expression level of Bip in the treated group was higher than the model group, while the mean gray were ( 121.17 ±4.76). The expression level of PERK and CHOP in the treated group was lower than the model group,while the mean gray were ( 122.11 ± 4.73 ), ( 123.34 ± 7.73 ) separately. Significant differences were observed between model group and aqueous extract of Broussonetia papyrifera ( L. ) Vent treated groups (P< 0. 05 ~ 0. 01 ).Conclusion Aqueous extract of Broussonetia papyrifera ( L. ) Vent can improve learning and memory disorders of the model rats induced by Aβ25-35 and D-galactose. ER (endoplasmic reticulum) stress and correlated apoptosis pathway might be involved in the underlying mechanisms. Key words: Alzheimer's disease; β-Amyloidal peptide25-35; D-galactose; ER stress; Broussonetia papyrifera (L.) Vent

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.