HPLC profile, biochemical and histoarchitectural changes in loperamide-induced constipated Wistar rats after oral administration of aqueous extract of Cnestis ferruginea (Vahl ex DC) roots

Abstract

Introduction

Aqueous extract of Cnestis ferruginea roots (AECFR) have been documented to exhibit laxative activity with no information on biochemical and histoarchitectural changes that accompany such treatments. Hence, this study was aimed at determining the biochemical and histoarchitectural alterations in constipated rats after treatment with AECFR.

Methodology

Sixty, healthy, Wistar rats (150.30 ± 3.52 g) were completely randomized into six groups (A-F; n = 10/group). Animals in group A (sham control, SC) received distilled water (DW) whilst constipated (induced with 3 daily doses of loperamide (LPD, 3 mg/kg body weight, BW) rats in groups B (negative control, NC), C (positive control, PC), D, E and F were orally gavaged at same point time with DW, bisacodyl (BCL, referenced cathartics, 25 mg/kg BW), AECFR at 25, 50 and 100 mg/kg BW, respectively, once daily for 7 days. Biochemical and histoarchitectural analyses/examinations and High Performance Liquid Chromatography (HPLC) profiling of AECFR were done using standard methods.

Results

The LPD-treatment related significant (p < 0.05) increases in liver ACP, liver and serum GGT, stomach and small intestine (SI) ALP, kidney AST, serum albumin (SALB), uric acid, urea, creatinine, TC, TAG, LDL-C and Cl^- were further sustained by AECFR and BCL. In contrast, the LPD-treatment related decreases in stomach ACP, serum globulin (SGB), total bilirubin (TB) and conjugated bilirubin (CB) were also reduced (p < 0.05) by the AECFR and BCL. Furthermore, the increases in the activities/levels of liver, kidney and serum ALP, liver and serum ALT, SI and serum ACP and HDL-C were reduced (p < 0.05) by the AECFR and BCL whereas the LPD-treatment related decreases in the activity/levels of kidney ALT, Na⁺, K⁺ and AI were increased after treatment with AECFR and BCL. In all, the alterations did not compare (p > 0.05) favourably with the SC. Also, there were no treatment-related histoarchitectural changes in all the tissues. Ten chemical compounds were detected in AECFR with cephatonine (30.96 µg/100 g) and stepharanine (0.13 µg/100 g) being the most and the least abundant respectively.

Conclusion

The LPD, AECFR and BCL caused similar trend of damage and/or cellular dysfunction to the liver, kidney, stomach and small intestine of rats with no evidence of histoarchitectural distortion in all the tissues.