3,4-Methylenedioxymethamphetamine causes retinal damage in C57BL/6J mice

2020 ◽  
Vol 39 (11) ◽  
pp. 1556-1564
Author(s):  
Y Ma ◽  
C Bian ◽  
D Song ◽  
G Yao ◽  
R Nie

3,4-Methylenedioxymethamphetamine (MDMA) is a powerfully addictive psychostimulant with pronounced effects on the central nervous system, but the precise mechanism of MDMA-induced toxicity remains unclear, specifically on the retina. This study was performed to investigate the effects of MDMA treatment on the retina and explore the underlying mechanism. C57BL/6J mice were randomly divided into control and MDMA groups. Mice were treated with MDMA at progressively increasing doses (1–6 mg/kg) intraperitoneally 4 times per day. Electroretinography was used to test the retinal function. Pathological changes of the retina were examined by toluidine blue staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay. Enzyme-linked immunosorbent assays were used to measure the levels of cytokines in the retina. Real-time polymerase chain reaction and Western blot were used to measure gene and protein expression in the retina, respectively. Our study showed that MDMA treatment impaired retinal function and decreased retinal thickness. MDMA treatment also increased transforming growth factor β as well as inflammatory factors in the retina. Moreover, MDMA treatment increased protein expression of matrix metalloproteinases (MMPs) and decreased tight junction protein expression in the retina. Our study indicated that treatment of MDMA caused retinal damage in C57BL/6J mice, associated with an increase of MMPs and a decrease of tight junction proteins.

2018 ◽  
Vol 37 (6) ◽  
pp. 448-456 ◽  
Author(s):  
Haojiang Yang ◽  
Liming Tao ◽  
Lin Li

As a powerful psychostimulant with high potential for abuse, methamphetamine (Meth) could cause long-lasting abnormalities in retinas. The purpose of this study was to investigate the effects of systemic administration of Meth at low dose on retinal damage and understand the underlying mechanisms of pathology. CD1 mice were treated with 0.5 mg/kg or 1 mg/kg Meth by intraperitoneal injection daily for 2 months, mice treated with saline were used as negative control. Electroretinography (ERG) reflects the mass response of photoreceptor cells and was used to test the outer retinal function after Meth treatment. Toluidine blue staining was used to show the retinal morphology and evaluate the photoreceptor cell loss. Inflammatory factors were measured by enzyme-linked immunosorbent assay to show the inflammatory response. Terminal deoxynucleotidyl transferase dUTP Nick end labeling assay was used to detect the apoptosis-positive cells. Real-time polymerase chain reaction and Western blot were applied to measure the gene and protein change to explore the underlying mechanisms. Results demonstrated that retinal damage was caused by Meth treatment after 2 months, evidenced by loss of rod photoreceptor cells; decreased ERG amplitude; increased apoptotic photoreceptor cells, cytochrome-c release, caspase-3 activity, caspase-9 activity, and apoptosis-related protein expression; increased malondialdehyde level as well as nicotinamide adenine dinucleotide phosphate oxidase 4 protein expression; decreased anti-oxidative agents glutathione as well as superoxide dismutase levels; and increased production and gene expression of inflammatory factors. Our study indicated that systemic administration of Meth caused neurotoxic effects on CD1 mouse retinas, providing the potential mechanisms for the retina damage caused by Meth abuse.


2016 ◽  
Vol 84 (1) ◽  
pp. 99-101 ◽  
Author(s):  
Seon-Pil Jin ◽  
Sang Bum Han ◽  
Yeon Kyung Kim ◽  
Elizabeth Eunkyung Park ◽  
Eun Jin Doh ◽  
...  

2018 ◽  
Vol 9 (6) ◽  
pp. 3321-3329 ◽  
Author(s):  
H. Wu ◽  
T. Luo ◽  
Y. M. Li ◽  
Z. P. Gao ◽  
K. Q. Zhang ◽  
...  

Granny Smith apple procyanidin extracts upregulate tight junction protein expression, probably acting via the modulation of oxidative stress and inflammation in lipopolysaccharide-induced Caco-2 cells.


2009 ◽  
Vol 72 (11) ◽  
pp. 868-877 ◽  
Author(s):  
Cristian M. Sobarzo ◽  
Livia Lustig ◽  
Roberto Ponzio ◽  
María Olga Suescun ◽  
Berta Denduchis

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