Ugbaja Regina Ngozi, Ogungbemi Kunle, James Adewale Segun, Peter Folorunsho Ayodele, Abolade Samuel Olanrewaju, Ajamikoko Stella Onajite, Atayese Eniola Olapeju, Adedeji Omowunmi Victoria
Department of Biochemistry, College of Bioscience, Federal University of Agriculture, P.M.B. 2240 Abeokuta, Nigeria.
Department of Chemistry/Biochemistry, Nigerian Stored Product Research Institute, P.M.B. 5044 Ibadan, Nigeria.
Pathophysiology. 2021 May 17;28(2):224-237. doi: 10.3390/pathophysiology28020015.
Hepato-renal dysfunctions associated with hyperlipidemia necessitates a continuous search for natural remedies. This study thus evaluated the effect of dietary chitosan on diet-induced hyperlipidemia in rats. A total of 30 male Wistar rats (90 ± 10) g were randomly allotted into six (6) groups ( = 5): Normal diet, High-fat diet (HFD), and Normal diet + 5% chitosan. The three other groups received HFD, supplemented with 1%, 3%, and 5% of chitosan. The feeding lasted for 6 weeks, after which the rats were sacrificed. The liver and kidneys were harvested for analyses. Hepatic alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activity, and renal biomarkers (ALT, AST, urea, and creatinine) were assayed spectrophotometrically. Additionally, expression of hepatic and renal CD43 and p53 was estimated immunohistochemically. The HFD group had elevated bodyweight compared to normal which was reversed in the chitosan-supplemented groups. Hyperlipidemia caused a significant ( < 0.05) decrease in the hepatic (AST, ALT, and ALP) and renal (AST and ALT) activities, while renal urea and creatinine increased. Furthermore, the HFD group showed an elevated level of hepatic and renal CD43 while p53 expression decreased. However, groups supplemented with chitosan showed improved hepatic and renal biomarkers, as well as corrected the aberrations in the expressions of p53 and CD43. Conclusively, dietary chitosan inclusion in the diet (between 3% and 5%) could effectively improve kidney and liver functionality via abatement of inflammatory responses.
与高脂血症相关的肝肾机能障碍使得人们需要不断寻找天然疗法。因此,本研究评估了膳食壳聚糖对大鼠饮食诱导的高脂血症的影响。总共30只体重为(90±10)克的雄性Wistar大鼠被随机分为六组(每组n = 5):正常饮食组、高脂饮食组(HFD)以及正常饮食+5%壳聚糖组。其他三组接受高脂饮食,并分别补充1%、3%和5%的壳聚糖。喂养持续6周,之后处死大鼠。采集肝脏和肾脏进行分析。采用分光光度法测定肝脏丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)活性以及肾脏生物标志物(ALT、AST、尿素和肌酐)。此外,通过免疫组织化学法评估肝脏和肾脏中CD43和p53的表达。与正常组相比,高脂饮食组体重升高,而在补充壳聚糖的组中体重升高的情况得到逆转。高脂血症导致肝脏(AST、ALT和ALP)和肾脏(AST和ALT)活性显著(P<0.05)降低,而肾脏尿素和肌酐升高。此外,高脂饮食组肝脏和肾脏CD43水平升高,而p53表达降低。然而,补充壳聚糖的组显示肝脏和肾脏生物标志物得到改善,并且纠正了p53和CD43表达的异常。总之,饮食中添加3%至5%的壳聚糖可通过减轻炎症反应有效改善肾脏和肝脏功能。