Hepatotoxicity and nephrotoxicity of saponin-enriched extract of Asparagus cochinchinensis in ICR mice.
- Author:
Ji Eun SUNG
1
;
Jun Young CHOI
;
Ji Eun KIM
;
Hyun Ah LEE
;
Woo Bin YUN
;
Jin Ju PARK
;
Hye Ryeong KIM
;
Bo Ram SONG
;
Dong Seob KIM
;
Chung Yeoul LEE
;
Hee Seob LEE
;
Yong LIM
;
Dae Youn HWANG
Author Information
- Publication Type:Original Article
- Keywords: Asparagus cochinchinensis; hepatotoxicity; nephrotoxicity; saponin; histopathology
- MeSH: Administration, Oral; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Blood Urea Nitrogen; Body Weight; Cell Line; Creatinine; Female; Humans; Kidney; L-Lactate Dehydrogenase; Liver; Male; Mice; Mice, Inbred ICR*; Models, Animal; Mortality; Organ Size; Pathology; Phenol; Phenotype; Saponins; Substance P
- From:Laboratory Animal Research 2017;33(2):57-67
- CountryRepublic of Korea
- Language:English
- Abstract: The inhibitory effects of Asparagus cochinchinensis against inflammatory response induced by lipopolysaccharide (LPS), substance P and phthalic anhydride (PA) treatment were recently reported for some cell lines and animal models. To evaluate the hepatotoxicity and nephrotoxicity of A. cochinchinensis toward the livers and kidneys of ICR mice, alterations in related markers including body weight, organ weight, urine composition, liver pathology and kidney pathology were analyzed in male and female ICR mice after oral administration of 150, 300 and 600 mg/kg body weight/day saponin-enriched extract of A. cochinchinensis (SEAC) for 14 days. The saponin, total flavonoid and total phenol levels were found to be 57.2, 88.5 and 102.1 mg/g in SEAC, respectively, and the scavenging activity of SEAC gradually increased in a dose-dependent manner. Moreover, body and organ weight, clinical phenotypes, urine parameters and mice mortality did not differ between the vehicle and SEAC treated group. Furthermore, no significant alterations were measured in alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and the serum creatinine (Cr) in the SEAC treated group relative to the vehicle treated group. Moreover, the specific pathological features induced by most toxic compounds were not observed upon liver and kidney histological analysis. Overall, the results of the present study suggest that SEAC does not induce any specific toxicity in the livers and kidneys of male and female ICR mice at doses of 600 mg/kg body weight/day.
