Le online two March 2022 Keywords and phrases: Depression Adult hippocampal neurogenesis Wnt/b-catenin CrocinPeer overview under responsibility of Cairo University. Corresponding authors at: School of Chinese Medicine, College of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Qixia District, Nanjing 210023, China (H. Zhang, Y. Hu). Interdisciplinary Institute for Customized Medicine in Brain Problems, and Study Center for Formula and Patterns, Jinan University, Huangpu Avenue, Guangzhou 510632, China (G. Chen). E-mail addresses: [email protected] (H. Zhang), [email protected] (Y. Hu), hdn_2001@126 (G. Chen). 1 These authors contributed equally to this work. doi.org/10.1016/j.jare.2022.02.015 2090-1232/2022 The Authors. Published by Elsevier B.V. on behalf of Cairo University. This can be an open access report under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).W. Tao, J. Ruan, R. Wu et al.Journal of Advanced Study 43 (2023) 219of glial fibrillary acidic protein (GFAP)-expressing newborn neural cells, temozolomide administration, microinfusion of Dkk1 or viral-mediated shRNA of Wnt3a. Outcomes: Crocin decreased the immobility duration in TST and FST without having impairing the performance in sexual behaviors. Crocin boosted the proliferation and differentiation of progenitors, and promoted dendritic maturation and functional integration of hippocampal newborn neurons. Conditional removal of GFAP-expressing neural cells or temozolomide administration impaired the antidepressant response of crocin. Moreover, Wnt/b-catenin signaling was promoted following crocin treatment. In chronic unpredictable mild anxiety (CUMS) murine model, crocin therapy displayed antidepressant response in SPT, FST and TST, and restored the neurogenesis levels and Wnt/b-catenin signaling impaired by CUMS. Infusion of Dickkopf-1 (DKK1) or knockdown of Wnt3a within the hippocampus impaired the antidepressant response of crocin. Conclusion: Crocin exerted antidepressant response, which was dependent on enhancement of AHN and activation of your Wnt/b-catenin pathway. 2022 The Authors. Published by Elsevier B.V. on behalf of Cairo University. This is an open access report below the CC BY-NC-ND license (http://creativecommons.DKK-3, Human (HEK293, His) org/licenses/by-nc-nd/4.Jagged-1/JAG1 Protein Biological Activity 0/).PMID:24455443 Introduction Major Depressive Disorder (MDD) can be a hugely prevalent illness which causes enormous society and economic burden around the world [1]. MDD impacts an individual’s quality of life and in some cases induces suicide [2]. Although monoamine-based antidepressants are widely made use of, slow-onset, low response prices and unwanted effects limit their clinical use [3]. Other options, fast-onset antidepressant therapies like sleep deprivation (SD) and low-dose ketamine also have many disadvantages, e.g., short duration of efficacy and unwanted side effects for instance headache and hallucination [4,5]. Therefore, it truly is essential to develop additional helpful and safer antidepressant treatment options. Adult hippocampal neurogenesis (AHN) acts as a essential role in hippocampal plasticity and is critically involved in mood regulation [6]. Neurogenesis persists all through life of mammals, primarily occurring in the subgranular zone (SGZ) and subventricular zone (SVZ) from the lateral ventricle in hippocampus [7]. These areas continuously proliferate neural stem cells (NSCs) and neural progenitor cells (NPCs), major to the generation of new neurons [8]. The adult neurogenesis in SGZ location is the highly multiple and compl.