2011国际外科学杂志Requires access

A newly proposed experimental liver fibrosis model induced by repeated injection of rabbits' liver homogenate in rats

Yi‐Yang Chen, Xin‐Min Li, Bao-en Wang, Xinyan Zhao

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Abstract

Objective To establish a method of a new type of liver fibrosis model in rats induced by repeated injection of rabbits' liver homogenate. Methods Female Wistar rats were randomly divided into a normal control group (8 rats), a human albumin induced liver fibrosis model group (15 rats) and a rabbits'liver homogenate induced liver fibrosis group (15 rats). The induction of liver fibrosis began with an immune sensitizing period (4 weeks) and was followed by an immune attacking period (8 weeks). After 8 weeks'attacking, all rats were sacrificed under anesthesia. Liver enzymes in serum and hydroxyproline in liver tissue were measured by standard methods and pathological scores were assessed by pathologists. Results The rats' liver weight, ratio of liver weight to body weight in the model group of liver homogenate were significantly increased compared with the normal control group. Serum globulin, tissue hydroxyproline were significantly increased, whereas serum albumin was significantly decreased in the homogenate group. There was only 20.0 percent of liver fibrosis score (2/10) exceeding a degree of 3 in the albumin group whereas 73.3 percent of that (11/15) were exceeding a degree of 3 in the homogenate group and the difference was significant (x2 = 4. 87,P = 0. 027). Conclusion In the study, we established a method of a new type of experimental liver fibrosis model in rats. The method has a significantly high success rate and this model can be used to study the mechanism of liver fibrosis and the efficacy of antifibrotic medicine. Key words: Liver fibrosis, experimental;  Liver homogenate;  Human albumin

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Objective To establish a method of a new type of liver fibrosis model in rats induced by repeated injection of rabbits' liver homogenate. Methods Female Wistar rats were randomly divided into a normal control group (8 rats), a human albumin induced liver fibrosis model group (15 rats) and a rabbits'liver homogenate induced liver fibrosis group (15 rats). The induction of liver fibrosis began with an immune sensitizing period (4 weeks) and was followed by an immune attacking period (8 weeks). After 8 weeks'attacking, all rats were sacrificed under anesthesia. Liver enzymes in serum and hydroxyproline in liver tissue were measured by standard methods and pathological scores were assessed by pathologists. Results The rats' liver weight, ratio of liver weight to body weight in the model group of liver homogenate were significantly increased compared with the normal control group. Serum globulin, tissue hydroxyproline were significantly increased, whereas serum albumin was significantly decreased in the homogenate group. There was only 20.0 percent of liver fibrosis score (2/10) exceeding a degree of 3 in the albumin group whereas 73.3 percent of that (11/15) were exceeding a degree of 3 in the homogenate group and the difference was significant (x2 = 4. 87,P = 0. 027). Conclusion In the study, we established a method of a new type of experimental liver fibrosis model in rats. The method has a significantly high success rate and this model can be used to study the mechanism of liver fibrosis and the efficacy of antifibrotic medicine. Key words: Liver fibrosis, experimental;  Liver homogenate;  Human albumin

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Available abstract

Objective To establish a method of a new type of liver fibrosis model in rats induced by repeated injection of rabbits' liver homogenate. Methods Female Wistar rats were randomly divided into a normal control group (8 rats), a human albumin induced liver fibrosis model group (15 rats) and a rabbits'liver homogenate induced liver fibrosis group (15 rats). The induction of liver fibrosis began with an immune sensitizing period (4 weeks) and was followed by an immune attacking period (8 weeks). After 8 weeks'attacking, all rats were sacrificed under anesthesia. Liver enzymes in serum and hydroxyproline in liver tissue were measured by standard methods and pathological scores were assessed by pathologists. Results The rats' liver weight, ratio of liver weight to body weight in the model group of liver homogenate were significantly increased compared with the normal control group. Serum globulin, tissue hydroxyproline were significantly increased, whereas serum albumin was significantly decreased in the homogenate group. There was only 20.0 percent of liver fibrosis score (2/10) exceeding a degree of 3 in the albumin group whereas 73.3 percent of that (11/15) were exceeding a degree of 3 in the homogenate group and the difference was significant (x2 = 4. 87,P = 0. 027). Conclusion In the study, we established a method of a new type of experimental liver fibrosis model in rats. The method has a significantly high success rate and this model can be used to study the mechanism of liver fibrosis and the efficacy of antifibrotic medicine. Key words: Liver fibrosis, experimental;  Liver homogenate;  Human albumin

Key concepts: Hydroxyproline, Liver fibrosis, Albumin, Internal medicine, Fibrosis, Medicine, Endocrinology, Globulin

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