Abstract
Hepatic encephalopathy (HE) is a neuropsychiatric disease that is developed as a complication of both acute and chronic liver failure affecting psychomotor dysfunction, memory, and concentration. This study is aimed at evaluating the therapeutic effects of Dunaliella salina (D. salina) microalgae in thioacetamide- (TAA-) induced HE in rats. HE was induced by TAA (200 mg/kg; i.p.) for three successive days. Forty male Wister albino rats were divided into 4 groups; the first group was served as a normal, and the second group was injected with TAA and served as TAA control. The third and fourth groups were administered D. salina (100 and 200 mg/kg; p.o.), respectively, after TAA injection for 7 days. The behavioral and biochemical markers as well as histological aspects of HE were estimated. This study revealed that TAA caused behavioral changes, oxidative stress, neuroinflammation, nuclear pyknosis, and neurons degeneration. D. salina improved liver function and decreased oxidative stress and inflammatory mediator as TLR4 protein expression. Also, D. salina elevated HSP-25 and IGF-1 as well as improved brain histopathological alterations. In conclusion, D. salina exerted a therapeutic potential against HE via its antioxidant, antiinflammatory and cytoprotective effects.
Highlights
Hepatic encephalopathy (HE) reflects a spectrum of neuropsychiatric abnormalities such as sensory abnormalities, psychomotor dysfunction, impaired memory, poor concentration, and increased reaction time
In order to give a better insight, we examined the role of hyperammonemia, oxidative stress, or inflammation pathways by which D. salina exerts its therapeutic actions in brain via Toll-like receptor 4 (TLR4), heat shock proteins (HSPs)-25, and insulin-like growth factor-1 (IGF-1) regulation
TAA injection resulted in a significant rise in serum ALT, AST, and ammonia levels by 83%, 72%, and 134%, respectively, when compared to the normal
Summary
Hepatic encephalopathy (HE) reflects a spectrum of neuropsychiatric abnormalities such as sensory abnormalities, psychomotor dysfunction, impaired memory, poor concentration, and increased reaction time. These manifestations are due to acute or chronic liver failure [1]. In HE, impaired liver function elevates the levels of ammonia in the blood that crosses the blood-brain barrier and metabolized in the CNS [4]. There is a cross talk between inflammatory mediators and ammonia in HE patients [7] such as toll-like receptors (TLRs), in acute or chronic hepatic diseases, that trigger inflammation [8] and act as critical determinants of HE severity via releasing proinflammatory mediators [9]. TLR4 activation mediates oxidative stress in neurons and hepatocytes [10]
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