Background and Objectives: Intraperitoneal injection (i.p.) of D-galactose (D-gal) accelerates aging and develops aging models. A low dose of long-term use and a high dose of short-term use of D-gal can induce natural aging in mice, like brain, cardiac, liver, renal, and skin aging, and erectile dysfunction. Our research aims to determine whether a high dose of short-term use of D-gal. i.p. in rats can induce natural aging and affect the following parameters: body weight (BW), Superoxide Dismutase (SOD), Vascular endothelial growth factor (VEGF), C-reactive protein (CRP), and myostatin. Methods: A daily D-gal i.p. dose of 300 mg/ml/kg for seven days was carried out to induce aging parameters in the rats. After seven days, the body and gastrocnemius circumference of the rats were weighed, and biochemical analysis for SOD, VEGF, CRP, and myostatin in the blood plasma was done. Results: The data obtained were analyzed using nonparametric statistics Friedman test and Mann-Whitney test. After the seven day-intervention, both the control (NaCl 0.9% i.p.) and the high dose of short-term use of D-gal i.p. groups showed no significant difference in the body weight and gastrocnemius circumference. However, D-gal administration could increase the blood plasma level of SOD, VEGF, CRP, and myostatin. Conclusion We conclude that a high dose of short-term intraperitoneal D-galactose can be administrated to induce aging in rat models. The SOD, VEGF, CRP and myostatin can be used as aging parameters.
Aging ; Galactose ; Myostatin ; Vascular Endothelial Growth Factor A

Background and Objectives: Intraperitoneal injection (i.p.) of D-galactose (D-gal) accelerates aging and develops aging models. A low dose of long-term use and a high dose of short-term use of D-gal can induce natural aging in mice, like brain, cardiac, liver, renal, and skin aging, and erectile dysfunction. Our research aims to determine whether a high dose of short-term use of D-gal. i.p. in rats can induce natural aging and affect the following parameters: body weight (BW), Superoxide Dismutase (SOD), Vascular endothelial growth factor (VEGF), C-reactive protein (CRP), and myostatin. Methods: A daily D-gal i.p. dose of 300 mg/ml/kg for seven days was carried out to induce aging parameters in the rats. After seven days, the body and gastrocnemius circumference of the rats were weighed, and biochemical analysis for SOD, VEGF, CRP, and myostatin in the blood plasma was done. Results: The data obtained were analyzed using nonparametric statistics Friedman test and Mann-Whitney test. After the seven day-intervention, both the control (NaCl 0.9% i.p.) and the high dose of short-term use of D-gal i.p. groups showed no significant difference in the body weight and gastrocnemius circumference. However, D-gal administration could increase the blood plasma level of SOD, VEGF, CRP, and myostatin. Conclusion We conclude that a high dose of short-term intraperitoneal D-galactose can be administrated to induce aging in rat models. The SOD, VEGF, CRP and myostatin can be used as aging parameters.
Aging ; D-Galactose ; Galactose ; Myostatin ; VEGF ; Vascular Endothelial Growth Factor A

Introduction: Hyperlipidemia is a condition that may lead to many illnesses. The worldwide prevalence of hyperlipidemia is still relatively high. Lactoferrin is a glycoprotein found in mammals and fishes’ epithelial mucosa cells, also known for its protective roles. Objective: This study aims to d Objective: This study aims to discover the histopathologic changes in rat’s liver after the intervention of 100, 200, and 400 mg/kgBW lactoferrin. Method: This study involved 30 Sprague-Dawley rats divided into six groups: normal, negative control, statin-treated, dose 1, dose 2, and dose 3. The normal group was given standard feed, while the other groups were hyperlipidemic induced by a high cholesterol diet. The intervention for the statin-treated group was 1.5 mg/kgBW statin, while dose 1, 2, and 3 were respectively given 100 mg/kgBW, 200 mg/kgBW, and 400 mg/kgBW of lactoferrin. After six weeks, all rats were dissected, and the livers’ histopathologic slides were scored with Manja Roenigk scoring. Result: Lactoferrin improved the fatty liver condition. The statistical test results showed that 200 mg/kgBW of lactoferrin caused a significant change in the rats’ liver structures (p < 0.05). Conclusion 200 mg/kgBW of lactoferrin significantly improved the histopathologic structure of fatty liver
Histology