Animal experimentation helps us to understand human biology. Rodents and, in particular, rats are among the most common animals used in animal experiments. Reporting data on animal age, animal body weight, and animal postnatal developmental stages is not consistent, which can cause the failure to translate animal data to humans. This review summarizes age-related postnatal developmental stages in rats by addressing age-related changes in their body weights. The age and body weight of animals can affect drug metabolism, gene expression, metabolic parameters, and other dependent variables measured in animal studies. In addition, considering the age and the body weight of the animals is of particular importance in animal modeling of human diseases. Appropriate reporting of age, body weight, and the developmental stage of animals used in studies can improve animal to human translation.

Decreased circulating levels of hydrogen sulfide (H₂S) are associated with higher mortality following myocardial ischemia. This study aimed at determining the long-term dose-dependent effects of sodium hydrosulfide (NaSH) administration on myocardial ischemia-reperfusion (IR) injury. Male rats were divided into control and NaSH groups that were treated for 9 weeks with daily intraperitoneal injections of normal saline or NaSH (0.28, 0.56, 1.6, 2.8, and 5.6 mg/kg), respectively. At the end of the study, hearts from all rats were isolated and hemodynamic parameters were recorded during baseline and following IR. In isolated hearts, infarct size, oxidative stress indices as well as mRNA expression of H₂S-, nitric oxide (NO)-producing enzymes, and inflammatory markers were measured. In heart tissue following IR, low doses of NaSH (0.28 and 0.56 mg/kg) had no effect, whereas an intermediate dose (1.6 mg/kg), improved recovery of hemodynamic parameters, decreased infarct size, and decreased oxidative stress. It also increased expression of cystathionine γ-lyase (CSE), Raf kinase inhibitor protein (RKIP), endothelial NO synthase (eNOS), and neuronal NOS (nNOS), as well as decreased expression of inducible NOS (iNOS) and nuclear factor kappa-B (NF-κB). At the high dose of 5.6 mg/kg, NaSH administration was associated with worse recovery of hemodynamic parameters and increased infarct size as well as increased oxidative stress. This dose also decreased expression of CSE, RKIP, and eNOS and increased expression of iNOS and NF-κB. In conclusion, chronic treatment with NaSH has a U-shaped concentration effect on IR injury in heart tissue. An intermediate dose was associated with higher CSE-derived H₂S, lower iNOS-derived NO, lower oxidative stress, and inflammation in heart tissue following IR.

Insulin resistance and inflammation are strongly linked to non-alcoholic fatty liver disease (NAFLD) as a feature of the metabolic syndrome. Furthermore, the role of dysregulation of miR-34a, miR-451, and miR-33a in pathogenesis and progression of NAFLD has been identified. trans-Chalcone is a simple chalcone with anti-diabetic and anti-inflammatory activities. However, to the best of our knowledge, miRNA-dependent mechanisms of these protective effects under pathologic conditions are not understood. Thus, this study, for the first time, aimed to evaluate the effects of trans-Chalcone on miR-34a, miR-451, and miR-33a signaling pathways in the liver of high-fat (HF) emulsion-fed rats. To this aim, twenty-one rats were randomly and equally divided into three groups: control, which was gavaged with 10% tween 80; HF, which was gavaged with HF emulsion and 10% tween 80; and HF + trans-Chalcone (HF + TC), which was gavaged with HF emulsion and trans-Chalcone. Then, circulating levels of glucose and insulin were measured and used for the calculation of HOMA-IR. Hepatic expression levels of miR-34a, miR-451, miR-33a, SIRT1, and ABCA1 and also protein levels of ABCA1 and IL-8 were assayed. In this study, trans-chalcone increased hepatic cholesterol efflux and prevented insulin resistance and liver inflammation in HF emulsion-fed rats. These protective effects were modulated through the down-regulation of miR-34a and its associated elevation of SIRT1, the up-regulation of miR-451 which was associated with a reduction in IL-8, and the inhibition of miR-33a which was related to the elevation of ABCA1 in the liver of HF emulsion-fed rats. Therefore, trans-Chalcone exerts its beneficial effects by targeting hepatic miR-34a-, miR-451-, and miR-33a-related pathways.