To the Editor:Major depressive disorder is one of the most leading causes of disability worldwide.The molecular pathophysiology of depression is complicated and has already attracted intensive and considerable attenti...To the Editor:Major depressive disorder is one of the most leading causes of disability worldwide.The molecular pathophysiology of depression is complicated and has already attracted intensive and considerable attentionj11 Nowadays,the neurotrophic hypothesis of depression suggests that brain-derived neurotrophic factor(BDNF)/tyrosine kinase receptor B(TrkB)receptor binding activates the downstream signaling pathways to culminate in cell survival.This process is essential for neurogenesis and synaptogenesis,which are involved in the effects of antidepressants.展开更多
Objective: Berberine, a cationic alkaloid first isolated in 1917, has been approved by the China Drug Administration for decades. Accumulating evidence demonstrated its antidepressant-like activities in vivo. Our prev...Objective: Berberine, a cationic alkaloid first isolated in 1917, has been approved by the China Drug Administration for decades. Accumulating evidence demonstrated its antidepressant-like activities in vivo. Our previous study has shown that chronic stress leads to the upregulation of miR-34a in the hippocampus of mice. This study aims to evaluate the underlying miR-34a mediated mechanism of berberine in chronic stress-induced depression in mice.Methods: In the present study, mice were administered with berberine during chronic stress. Levels of miR-34a, dendritic density, mitochondrial morphology, and neurogenesis were assessed in the hippocampus. Subsequently, miR-34a agomir was used as a pharmacological intervention for the investigation of berberine.Results: The results showed that berberine reversed the decrease in sucrose preference and the increase in latency to feed without altering total food consumption. Furthermore, chronic stress-induced overexpression of miR-34a decreased synaptotagmin-1 and Bcl-2 levels, thereby impairing spinal morphology,mitochondria and neurogenesis. Berberine inhibited miR-34a expression, in turn restored synaptotagmin-1 and Bcl-2 levels, and thus improved spinal morphology, mitochondria and neurogenesis in the hippocampus. However, the improvements induced by berberine were totally blocked by the pretreatment of miR-34a agomir, which caused the elevation of miR-34a levels in the hippocampus.Conclusion: This finding demonstrated that miR-34a downregulation was involved in the antidepressantlike effects of berberine in mice exposed to chronic stress.展开更多
基金grants from the Education Department of Fujian Province[No.2019-WJ-38]Xiamen Municipal Health Commission[No.2019-WJ-38]Huaqiao University[No.ZQN-PY218].
文摘To the Editor:Major depressive disorder is one of the most leading causes of disability worldwide.The molecular pathophysiology of depression is complicated and has already attracted intensive and considerable attentionj11 Nowadays,the neurotrophic hypothesis of depression suggests that brain-derived neurotrophic factor(BDNF)/tyrosine kinase receptor B(TrkB)receptor binding activates the downstream signaling pathways to culminate in cell survival.This process is essential for neurogenesis and synaptogenesis,which are involved in the effects of antidepressants.
基金the Education Department of Fujian Province [2019-WJ-38]Xiamen Municipal Health Commission [2019-WJ-38]。
文摘Objective: Berberine, a cationic alkaloid first isolated in 1917, has been approved by the China Drug Administration for decades. Accumulating evidence demonstrated its antidepressant-like activities in vivo. Our previous study has shown that chronic stress leads to the upregulation of miR-34a in the hippocampus of mice. This study aims to evaluate the underlying miR-34a mediated mechanism of berberine in chronic stress-induced depression in mice.Methods: In the present study, mice were administered with berberine during chronic stress. Levels of miR-34a, dendritic density, mitochondrial morphology, and neurogenesis were assessed in the hippocampus. Subsequently, miR-34a agomir was used as a pharmacological intervention for the investigation of berberine.Results: The results showed that berberine reversed the decrease in sucrose preference and the increase in latency to feed without altering total food consumption. Furthermore, chronic stress-induced overexpression of miR-34a decreased synaptotagmin-1 and Bcl-2 levels, thereby impairing spinal morphology,mitochondria and neurogenesis. Berberine inhibited miR-34a expression, in turn restored synaptotagmin-1 and Bcl-2 levels, and thus improved spinal morphology, mitochondria and neurogenesis in the hippocampus. However, the improvements induced by berberine were totally blocked by the pretreatment of miR-34a agomir, which caused the elevation of miR-34a levels in the hippocampus.Conclusion: This finding demonstrated that miR-34a downregulation was involved in the antidepressantlike effects of berberine in mice exposed to chronic stress.
