Objective Anesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neu...Objective Anesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rb1 can attenuate isoflurane/surgery-induced cognitive dysfunction via inhibiting neuroinflammation and oxidative stress. Methods Five-months-old C57BL/6J female mice were treated with 1.4% isoflurane plus abdominal surgery for two hours. Sixty mg/kg ginsenoside Rb1 were given intraperitoneally from 7 days before surgery. Cognition of the mice were assessed by Barnes Maze. Levels of postsynaptic density-95 and synaptophysin in mice hippocampus were measured by Western blot. Levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in mice hippocampus were measured by ELISA. Results Here we show for the first time that the ginsenoside Rb1 treatment attenuated the isoflurane/surgery-induced cognitive impairment. Moreover, ginsenoside Rb1 attenuated the isoflurane/surgery-induced synapse dysfunction. Finally, ginsenoside Rb1 mitigated the isoflurane/surgery-induced elevation levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in the mice hippocampus. Conclusion These results suggest that ginsenoside Rb1 may attenuate the isoflurane/surgery-induced cognitive impairment by inhibiting neuroinflammation and oxidative stress pending future studies.展开更多
Parkinson’s disease(PD)is one of the most common neurodegenerative diseases with a complex pathogenesis.Aggregations formed by abnormal deposition of alpha-synuclein(αSyn)lead to synapse dysfunction of the dopamine ...Parkinson’s disease(PD)is one of the most common neurodegenerative diseases with a complex pathogenesis.Aggregations formed by abnormal deposition of alpha-synuclein(αSyn)lead to synapse dysfunction of the dopamine and non-dopamine systems.The loss of dopaminergic neurons and concomitant alterations in non-dopaminergic function in PD constitute its primary pathological manifestation.Positron emission tomography(PET),as a representative molecular imaging technique,enables the non-invasive visualization,characterization,and quantification of biological processes at cellular and molecular levels.Imaging synaptic function with PET would provide insights into the mechanisms underlying PD and facilitate the optimization of clinical management.In this review,we focus on the synaptic dysfunction associated with theαSyn pathology of PD,summarize various related targets and radiopharmaceuticals,and discuss applications and perspectives of PET imaging of synaptic dysfunction in PD.展开更多
文摘Objective Anesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rb1 can attenuate isoflurane/surgery-induced cognitive dysfunction via inhibiting neuroinflammation and oxidative stress. Methods Five-months-old C57BL/6J female mice were treated with 1.4% isoflurane plus abdominal surgery for two hours. Sixty mg/kg ginsenoside Rb1 were given intraperitoneally from 7 days before surgery. Cognition of the mice were assessed by Barnes Maze. Levels of postsynaptic density-95 and synaptophysin in mice hippocampus were measured by Western blot. Levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in mice hippocampus were measured by ELISA. Results Here we show for the first time that the ginsenoside Rb1 treatment attenuated the isoflurane/surgery-induced cognitive impairment. Moreover, ginsenoside Rb1 attenuated the isoflurane/surgery-induced synapse dysfunction. Finally, ginsenoside Rb1 mitigated the isoflurane/surgery-induced elevation levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in the mice hippocampus. Conclusion These results suggest that ginsenoside Rb1 may attenuate the isoflurane/surgery-induced cognitive impairment by inhibiting neuroinflammation and oxidative stress pending future studies.
基金supported by the National Key Research and Development Program of China(2022YFC2009900,2021YFE0108300,2022YFE0118000,and 2021YFA1101700)the National Natural Science Foundation of China(82030049)Fundamental Research Funds for the Central Universities of China.
文摘Parkinson’s disease(PD)is one of the most common neurodegenerative diseases with a complex pathogenesis.Aggregations formed by abnormal deposition of alpha-synuclein(αSyn)lead to synapse dysfunction of the dopamine and non-dopamine systems.The loss of dopaminergic neurons and concomitant alterations in non-dopaminergic function in PD constitute its primary pathological manifestation.Positron emission tomography(PET),as a representative molecular imaging technique,enables the non-invasive visualization,characterization,and quantification of biological processes at cellular and molecular levels.Imaging synaptic function with PET would provide insights into the mechanisms underlying PD and facilitate the optimization of clinical management.In this review,we focus on the synaptic dysfunction associated with theαSyn pathology of PD,summarize various related targets and radiopharmaceuticals,and discuss applications and perspectives of PET imaging of synaptic dysfunction in PD.
