Study of anesthetics for euthanasia in rats and mice: A systematic review and meta-analysis on the impact upon biological outcomes (SAFE-RM)

Leitão, Santiago Alonso Tobar; Soares, Douglas dos Santos; Carvas, Nelson; Zimmer, Rafael; Ludwig, Nataniel Floriano; Andrades, Michael Éverton

doi:10.1016/j.lfs.2021.119916

Cited by 8 publications

(2 citation statements)

References 31 publications

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“…Barbiturates may have effects on physiological parameters and the recovery is marked by a prolonged period before full consciousness is restored. Therefore, the use of different anaesthetics imposes limitations when comparing studies [ 29 ]. Another limitation was the use of crystalloid during resuscitation.…”

Section: Discussionmentioning

confidence: 99%

Doxycycline reduces liver and kidney injuries in a rat hemorrhagic shock model

Sordi,

Bojko,

Oliveira

et al. 2024

ICMx

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Background Hemorrhagic shock (HS), which causes insufficient tissue perfusion, can result in multiple organ failure (MOF) and death. This study aimed to evaluate whether doxycycline (DOX) protects cardiovascular, kidney, and liver tissue from damage in a rat model of HS. Immediately before the resuscitation, DOX (10 mg/kg; i.v.) was administered, and its protective effects were assessed 24 h later. Mean arterial pressure, renal blood flow, heart rate, vasoactive drug response, and blood markers such as urea, creatinine, AST, ALT, CPK, CPR, and NOx levels were determined. Results We showed that DOX has a significant effect on renal blood flow and on urea, creatinine, AST, ALT, CPK, and NOx. Morphologically, DOX reduced the inflammatory process in the liver tissue. Conclusions We conclude that DOX protects the liver and kidney against injury and dysfunction in a HS model and could be a strategy to reduce organ damage associated with ischemia-and-reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

Doxycycline reduces liver and kidney injuries in a rat hemorrhagic shock model

Sordi,

Bojko,

Oliveira

et al. 2024

ICMx

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“…Juvenile male SD rats in the 5-, 10-, and 20-day-old groups ( n = 3–5 each) were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The juvenile rats were sacrificed under pentobarbital sodium (5.4 g/kg) treatment [ 25 , 26 ]. We quickly dissected and opened the abdominal and chest cavities; collected the heart, lung, and liver; and washed them with phosphate-buffered saline (PBS) at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Changes in glutamic oxaloacetic transaminase 2 during rat physiological and pathological cardiomyocyte hypertrophy

Liu,

Li,

Zhou

2023

BMC Cardiovasc Disord

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Background Physiological and pathological cardiomyocyte hypertrophy are important pathophysiological processes of adult congenital heart disease-associated ventricular hypertrophy. Glutamic oxaloacetic transaminase (GOT) is a vital marker of myocardial injury. This study aimed to investigate the changes in GOT levels during physiological and pathological cardiomyocyte hypertrophy in rats. Methods RNA-seq analysis and colorimetric methods were used to evaluate the changes in GOT mRNA and activity, respectively. GOT2 protein expression was detected by western blotting and immunofluorescence. Hematoxylin-eosin and wheat germ agglutinin methods were used to observe changes in rat cardiomyocyte morphology. Results In juvenile rat hearts, GOT mRNA expression and activity, and GOT2 protein level increased with age-related physiological cardiomyocyte hypertrophy; however, GOT2 protein level was reduced in hypoxia-induced pathological cardiomyocyte hypertrophy. Conclusions GOT2 may regulate physiological and pathological myocardial hypertrophy in rats. We speculated that the low GOT2 level contributed to the rapid occurrence of pathological cardiomyocyte hypertrophy, causing strong plasticity of right ventricular cardiomyocytes in the early postnatal period and heart failure in adulthood.

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Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cells

et al. 2022

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The de novo lipogenesis (DNL) pathway has been identified as a regulator of cancer progression and aggressiveness. Downregulation of key lipogenesis enzymes has been shown to activate apoptosis in cancerous cells. Epigallocatechin gallate (EGCG) inhibits cancer cell proliferation without causing cytotoxicity in healthy cells. The present study aimed to investigate the effects of EGCG on the promotion of apoptosis associated with the DNL pathway inhibition in cancer cells, both in vitro and in vivo. We observed that two colorectal cancer cell lines (HCT116 and HT‐29) had a higher cytotoxic response to EGCG treatment than hepatocellular carcinoma cells, including HepG2 and HuH‐7. EGCG treatment decreased cell viability and increased mitochondrial damage‐triggered apoptosis in both HCT116 and HT‐29 cancer cells. Additionally, we treated mice transplanted with HCT116 cells with 30 or 50 mg·kg−1 EGCG for 7 days to evaluate the apoptotic effects of EGCG treatment in a xenograft mouse model of cancer. We observed a decrease in intracellular fatty acid levels, which suggested that EGCG‐induced apoptosis was associated with a decrease in fatty acid levels in cancer. Suppression of ATP synthesis by EGCG indicated that cell death induction in cancer cells could be mediated by shared components of the DNL and energy metabolism pathways. In addition, EGCG‐induced apoptosis suppressed the expression of the phosphorylation protein kinase B and extracellular signal‐regulated kinase 1/2 signaling proteins in tumors from xenografted mice. Cytotoxic effects in unaffected organs and tissues of the mouse xenograft model were absent upon EGCG treatment.

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Study of anesthetics for euthanasia in rats and mice: A systematic review and meta-analysis on the impact upon biological outcomes (SAFE-RM)

Cited by 8 publications

References 31 publications

Doxycycline reduces liver and kidney injuries in a rat hemorrhagic shock model

Doxycycline reduces liver and kidney injuries in a rat hemorrhagic shock model

Changes in glutamic oxaloacetic transaminase 2 during rat physiological and pathological cardiomyocyte hypertrophy

Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cells

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