Abstract

The current work assessed the preventive and therapeutic potential of Hibiscus sabdariffa “HS” aqueous extract (HSE) on thioacetamide (TAA)-induced hepatic encephalopathy (HE) associated with the acute liver injury. Method: guinea pigs were divided into: Group 1 (Control group n=24) which wasfurther subdivided into 4 subgroups; Group “1-a” (non-treated); Group “1-b” given HSE for 3 days and sacrificed on the 4th day; Group “1-c” given TAA for 3 days and sacrificed on the 4th day; Group “1-d” given the TAA doses for 3 days and sacrificed on the 7th day; Group 2 (Preventive) given TAA and HSE doses concurrently for 3 days and sacrificed on the 4th day. Group 3 (Therapeutic) given 3-days TAA followed by 3-days HSE doses and sacrificed on the 7th day. Results: Preventive and therapeutic HSE resulted in significant amelioration of the TAA-induced hepatic encephalopathy with faster recovery of animals on the 7th day associated with significant improvement in the biochemical parameters of liver injury including the ammonia extraction ratio indicating functional hepatic improvement. In addition, there was a significant improvement in brain edema. Conclusion: HSE has both preventive and therapeutic effects on TAA-induced hepatic encephalopathy and liver injury in guinea pigs

Highlights

  • Hepatic encephalopathy (HE) is one of the most serious complications of hepatic failure, either acute or chronic

  • Administration of Hibiscus sabdariffa (HS)” aqueous extract (HSE) to normal animals in group “1-b” showed comparable results to that of the animals of the non-treated control group “1-a” without significant differences denoting no apparent effect of HSE (250 mg/kg/d) on the normal guinea pigs’ liver and brain

  • The results of the current study demonstrate that HSE treatment has both protective and therapeutic effects evidenced by attenuating the manifestations of hepatic encephalopathy induced by i.p. thioacetamide injection in guinea pigs and hastening their recovery

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Summary

Introduction

Hepatic encephalopathy (HE) is one of the most serious complications of hepatic failure, either acute or chronic. Most patients with cirrhosis show a spectrum of reversible neuropsychiatric symptoms during the course of their disease, with up to 25% developing overt HE within 5 years after cirrhosis diagnosis and up to 80% developing minimal HE (Ridola et al 2018). In addition to death risk, hepatic encephalopathy is associated with poor quality of life, impaired daily activity, decreased work productivity and frequent hospitalization for the treatment of recurrent episodes (Munoz, 2008). Treatment that lowers blood ammonia level can improve symptoms of hepatic encephalopathy (Munoz, 2008). Many other factors have been mentioned including oxidative stress, endogenous benzodiazepine-like ligands, astrocyte swelling, abnormal neurotransmission, neurosteroids and γ-aminobutyric acid–like molecules, inflammatory cytokines and others (Butterworth 2015)

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