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Environmental enrichment and abstinence attenuate ketamine-induced cardiac and renal toxicity.

Li X, Li S, Zheng W, Pan J, Huang K, Chen R, Pan T, Liao G, Chen Z, Zhou D, Shen W, Zhou W, Liu Y - Sci Rep (2015)

Bottom Line: Two weeks of ketamine SA caused significant increases in organ weight, Apoptosis Stimulating Fragment/Kidney Injury Molecule-1, and apoptotic level of heart and kidney.The extended length of withdrawal from ketamine SA partially reduced toxicity on the heart and kidney.The interactive effect of EE and abstinence was promising to promote the recovery of cardiac and renal toxicity of ketamine.

View Article: PubMed Central - PubMed

Affiliation: Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, Zhejiang 315211, P. R. China.

ABSTRACT
The current study was designed to investigate the effect of abstinence in combination with environmental enrichment (EE) on cardiac and renal toxicity induced by 2 weeks of ketamine self-administration (SA) in rodents. In Experiment 1, one group of rats underwent ketamine SA for 14 days. In Experiment 2, the animals completed 2 weeks of ketamine SA followed by 2 and 4 weeks of abstinence. In Experiment 3, animals underwent 14 days of ketamine SA and 4 weeks of abstinence in which isolated environment (IE) and EE was introduced. The corresponding control groups were included for each experiment. Two weeks of ketamine SA caused significant increases in organ weight, Apoptosis Stimulating Fragment/Kidney Injury Molecule-1, and apoptotic level of heart and kidney. The extended length of withdrawal from ketamine SA partially reduced toxicity on the heart and kidney. Finally, introduction of EE during the period of abstinence greatly promoted the effect of abstinence on ketamine-induced cardiac and renal toxicity. The interactive effect of EE and abstinence was promising to promote the recovery of cardiac and renal toxicity of ketamine.

No MeSH data available.


Related in: MedlinePlus

Effects of ketamine SA on morphological alterations and toxicity of the kidney.(A,B) Representative images of H&E staining for a saline and a ketamine SA rat. Arrow represents tubular atrophy. (C,D) Representative images of IHC staining for a saline and a ketamine SA rat. Arrow represents a cell with positive expression of KIM-1. (E) KIM-1 levels for saline (left) and ketamine SA (right) groups (F,G) Representive TUNEL staining images for a saline (left) and a ketamine SA (right) rat. (H) TUNEL + cells (%) for saline (left) and ketamine SA (right) groups. Arrow represents an apoptotic cell. Data are expressed as mean ± SEM. ** p < 0.01. SA: self-administration; KIM-1: kidney injury molecule 1; TUNEL: Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The KIM-1 level was defined as the average integral optical density.
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f3: Effects of ketamine SA on morphological alterations and toxicity of the kidney.(A,B) Representative images of H&E staining for a saline and a ketamine SA rat. Arrow represents tubular atrophy. (C,D) Representative images of IHC staining for a saline and a ketamine SA rat. Arrow represents a cell with positive expression of KIM-1. (E) KIM-1 levels for saline (left) and ketamine SA (right) groups (F,G) Representive TUNEL staining images for a saline (left) and a ketamine SA (right) rat. (H) TUNEL + cells (%) for saline (left) and ketamine SA (right) groups. Arrow represents an apoptotic cell. Data are expressed as mean ± SEM. ** p < 0.01. SA: self-administration; KIM-1: kidney injury molecule 1; TUNEL: Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The KIM-1 level was defined as the average integral optical density.

Mentions: Ketamine SA exerted toxicity on kidney. The H&E staining results showed that the Ketamine SA group had a greater infiltration of mononuclear cells and tubular atrophy, compared with the corresponding control group (Fig. 3A,B). Moreover, tubules appeared to be distorted and blocked (Fig. 3A,B). Independent t-test revealed that the level of Kidney Injury Molecule-1 (KIM-1) was significantly increased in the Ketamine SA group, compared with the corresponding control group (p < 0.01; Fig. 3C–E). Lastly, ketamine SA produced a significant increase in the number of TUNEL + cells in kidney, relative to the corresponding control group (p < 0.01; Fig. 3F–H).


Environmental enrichment and abstinence attenuate ketamine-induced cardiac and renal toxicity.

Li X, Li S, Zheng W, Pan J, Huang K, Chen R, Pan T, Liao G, Chen Z, Zhou D, Shen W, Zhou W, Liu Y - Sci Rep (2015)

Effects of ketamine SA on morphological alterations and toxicity of the kidney.(A,B) Representative images of H&E staining for a saline and a ketamine SA rat. Arrow represents tubular atrophy. (C,D) Representative images of IHC staining for a saline and a ketamine SA rat. Arrow represents a cell with positive expression of KIM-1. (E) KIM-1 levels for saline (left) and ketamine SA (right) groups (F,G) Representive TUNEL staining images for a saline (left) and a ketamine SA (right) rat. (H) TUNEL + cells (%) for saline (left) and ketamine SA (right) groups. Arrow represents an apoptotic cell. Data are expressed as mean ± SEM. ** p < 0.01. SA: self-administration; KIM-1: kidney injury molecule 1; TUNEL: Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The KIM-1 level was defined as the average integral optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4481381&req=5

f3: Effects of ketamine SA on morphological alterations and toxicity of the kidney.(A,B) Representative images of H&E staining for a saline and a ketamine SA rat. Arrow represents tubular atrophy. (C,D) Representative images of IHC staining for a saline and a ketamine SA rat. Arrow represents a cell with positive expression of KIM-1. (E) KIM-1 levels for saline (left) and ketamine SA (right) groups (F,G) Representive TUNEL staining images for a saline (left) and a ketamine SA (right) rat. (H) TUNEL + cells (%) for saline (left) and ketamine SA (right) groups. Arrow represents an apoptotic cell. Data are expressed as mean ± SEM. ** p < 0.01. SA: self-administration; KIM-1: kidney injury molecule 1; TUNEL: Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. The KIM-1 level was defined as the average integral optical density.
Mentions: Ketamine SA exerted toxicity on kidney. The H&E staining results showed that the Ketamine SA group had a greater infiltration of mononuclear cells and tubular atrophy, compared with the corresponding control group (Fig. 3A,B). Moreover, tubules appeared to be distorted and blocked (Fig. 3A,B). Independent t-test revealed that the level of Kidney Injury Molecule-1 (KIM-1) was significantly increased in the Ketamine SA group, compared with the corresponding control group (p < 0.01; Fig. 3C–E). Lastly, ketamine SA produced a significant increase in the number of TUNEL + cells in kidney, relative to the corresponding control group (p < 0.01; Fig. 3F–H).

Bottom Line: Two weeks of ketamine SA caused significant increases in organ weight, Apoptosis Stimulating Fragment/Kidney Injury Molecule-1, and apoptotic level of heart and kidney.The extended length of withdrawal from ketamine SA partially reduced toxicity on the heart and kidney.The interactive effect of EE and abstinence was promising to promote the recovery of cardiac and renal toxicity of ketamine.

View Article: PubMed Central - PubMed

Affiliation: Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, Zhejiang 315211, P. R. China.

ABSTRACT
The current study was designed to investigate the effect of abstinence in combination with environmental enrichment (EE) on cardiac and renal toxicity induced by 2 weeks of ketamine self-administration (SA) in rodents. In Experiment 1, one group of rats underwent ketamine SA for 14 days. In Experiment 2, the animals completed 2 weeks of ketamine SA followed by 2 and 4 weeks of abstinence. In Experiment 3, animals underwent 14 days of ketamine SA and 4 weeks of abstinence in which isolated environment (IE) and EE was introduced. The corresponding control groups were included for each experiment. Two weeks of ketamine SA caused significant increases in organ weight, Apoptosis Stimulating Fragment/Kidney Injury Molecule-1, and apoptotic level of heart and kidney. The extended length of withdrawal from ketamine SA partially reduced toxicity on the heart and kidney. Finally, introduction of EE during the period of abstinence greatly promoted the effect of abstinence on ketamine-induced cardiac and renal toxicity. The interactive effect of EE and abstinence was promising to promote the recovery of cardiac and renal toxicity of ketamine.

No MeSH data available.


Related in: MedlinePlus