Wenru Tian
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Wenru Tian has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Bilin Yang
Department of Children’s and Adolescent Health, Public Health College of Harbin Medical University, Harbin, China
1 shared publication - Caihong Sun
Department of Children's and Adolescent Health, Public Health College, Harbin Medical University, Harbin, China
1 shared publication - Caiyao Du
Department of Children’s and Adolescent Health, Public Health College of Harbin Medical University, Harbin, China
1 shared publication - Di Liu
School of Marxism, Harbin Medical University, Harbin, China
1 shared publication - Huirong Liang
Department of Children’s and Adolescent Health, Public Health College of Harbin Medical University, Harbin, China
1 shared publication - Lijie Wu
Department of Children's and Adolescent Health, Public Health College Harbin Medical University Harbin China
1 shared publication
Latest Publications
- 6 November 2024
- Published by Springer Nature in Molecular Neurobiology
- Vol. 62 (4) , 5022-5038
Augmentation of Endogenous 2-Arachidonoylglycerol Mitigates Autistic Behaviors of BTBR Mice
The lipid-based endocannabinoid (eCB) system regulates a host of developmental, physiological, and pathological processes in the mammalian brain, and recent studies have suggested that dysfunction of eCB system may contribute to the neuropathology of autism spectrum disorder (ASD). However, specific contributions to ASD-related developmental, cognitive, and behavioral phenotypes remain largely unexplored. The current study was designed to investigate if enhancing eCB signaling by blocking 2-arachidonoylglycerol (2-AG) hydrolase can mitigate ASD-like behaviors in a mouse model, and if such effects are associated with suppression of inflammatory signaling, oxidative stress, or neuronal apoptosis. Intraperitoneal injection of the 2-AG hydrolase monoacylglycerol lipase (MAGL) JZL184 (4, 16, or 40 mg/kg) elevated 2-AG and reversed eCB system metabolic enzymes and receptors expression deficits in BTBR T + ltpr3tf/J (BTBR) mouse model of ASD. Moreover, the hyperactivity, excessive stereotypy, impaired social behavior, and cognitive deficits characteristic of this animal model were significantly improved by JZL184. Concomitantly, JZL184 administration reversed the abnormal pro- and anti-inflammatory cytokine concentrations measured in the hippocampus of BTBR mice. In addition, JZL184 reversed the observed overexpression of pro-apoptotic Bax and underexpression of anti-apoptotic Bcl-2 in BTBR mice and enhanced neuronal numbers in hippocampal CA1 and CA3 regions. We also found that the behavioral test battery influenced eCB concentrations independently of JZL184 treatment. Collectively, these findings suggest that augmenting eCB signaling can mitigate ASD-related phenotypes by suppressing neuroinflammation and neuronal apoptosis.
- 6 November 2024
- Published by Springer Nature in Molecular Neurobiology
- Vol. 62 (4) , 5022-5038
Augmentation of Endogenous 2-Arachidonoylglycerol Mitigates Autistic Behaviors of BTBR Mice
The lipid-based endocannabinoid (eCB) system regulates a host of developmental, physiological, and pathological processes in the mammalian brain, and recent studies have suggested that dysfunction of eCB system may contribute to the neuropathology of autism spectrum disorder (ASD). However, specific contributions to ASD-related developmental, cognitive, and behavioral phenotypes remain largely unexplored. The current study was designed to investigate if enhancing eCB signaling by blocking 2-arachidonoylglycerol (2-AG) hydrolase can mitigate ASD-like behaviors in a mouse model, and if such effects are associated with suppression of inflammatory signaling, oxidative stress, or neuronal apoptosis. Intraperitoneal injection of the 2-AG hydrolase monoacylglycerol lipase (MAGL) JZL184 (4, 16, or 40 mg/kg) elevated 2-AG and reversed eCB system metabolic enzymes and receptors expression deficits in BTBR T + ltpr3tf/J (BTBR) mouse model of ASD. Moreover, the hyperactivity, excessive stereotypy, impaired social behavior, and cognitive deficits characteristic of this animal model were significantly improved by JZL184. Concomitantly, JZL184 administration reversed the abnormal pro- and anti-inflammatory cytokine concentrations measured in the hippocampus of BTBR mice. In addition, JZL184 reversed the observed overexpression of pro-apoptotic Bax and underexpression of anti-apoptotic Bcl-2 in BTBR mice and enhanced neuronal numbers in hippocampal CA1 and CA3 regions. We also found that the behavioral test battery influenced eCB concentrations independently of JZL184 treatment. Collectively, these findings suggest that augmenting eCB signaling can mitigate ASD-related phenotypes by suppressing neuroinflammation and neuronal apoptosis.