Hepatotoxicity refers to the deterioration in liver function brought
about by pharmacological chemical side effects. Hepatotoxicity is
frequently brought on by a wide range of pharmaceutical drugs and
environmental pollutants. Hepatotoxins are the substance that harms the
liver. Hepatotoxic drugs and chemicals have the potential to damage the
liver through several mechanisms, including mitochondrial dysfunction,
causing the death of the liver cells, and disrupting liver metabolism.
Some hepatotoxic drugs and chemicals, such as carbon tetrachloride,
paracetamol, mercury, cadmium, erythromycin, ranitidine, etc causing
hepatic damage by different ways. Hepatotoxicity is steadily rising in
occurrence and is becoming a major cause of death on a global scale.
Although there are numerous allopathic and traditional therapies that
provide hepatoprotection, treating chronic liver disease remains
difficult for medical practitioners. Rodents are frequently employed in
the lab for inducing hepatotoxicity for this reason. Hepatic toxicity is
typically induced by non-invasive techniques such as high-fat diets,
alcohol, radiation, toxic medications (NSAIDs, antibiotics, and
chemotherapeutic treatments), harmful metals (mercury, arsenic, lead,
and cadmium), and harmful substances (CCL4, thioacetamide, aflatoxin B1,
etc.).Portal vein ligation and bile duct ligation are two common
invasive procedures.
Background
Neuroprotective effect of silymarin against 3‐nitropropionic acid‐induced Huntington’s like symptoms in rats.
Method
Huntington's disease (HD) is a chronic neurodegenerative and hyperkinetic movement disorder characterized by degeneration of GABAergic medium spiny neurons, mainly affecting striatum and cortex. 3‐nitropropionic acid (3‐NP) acts as a suitable animal model to induce HD like symptoms in rats. Therefore, the present study aimed to investigate the neuroprotective effect of silymarin against 3‐NP induced HD like symptoms in rats. Rats were administered 3‐NP (10 mg/kg; i.p) for 21 days, whereas silymarin (50, 100 and 200 mg/kg; p.o) was given once a day, 1 hour before the 3‐NP treatment for 21 days. Body weight and behavioral parameters (rotarod, open field test, and narrow beam walk activities) were assessed on 1st, 7th, 14th, and 21st days. On the 22nd day, the animals were sacrificed, and the rat striatum and cortex were isolated to perform biochemical parameters (lipid peroxidation; glutathione; superoxide dismutase; nitrite and catalase).
Result
Systemic 3‐NP treatment significantly reduced body weight, motor‐coordination, and oxidative defense. Pretreatment with silymarin significantly attenuated the 3‐NP induced alterations in body weight, locomotor activities, and oxidative defense.
Conclusion
Our results revealed that in a 3‐NP model of HD, silymarin could underlie the possible neuroprotective effect, which may provide insight into the therapeutic potential of silymarin for HD.
BackgroundAlzheimer’s disease (AD) is an age related neurodegenerative disease mainly characterized by progressive cognitive decline, synaptic loss, extracellular amyloid‐beta (Aβ) deposits and intracellular accumulation of neurofibrillary tangles of tau protein. Multiple etiological factors have been linked with AD pathophysiology, oxidative stress, neuroinflammation, neurotransmitter deficit and foremost are the deregulation of lipid metabolism, consistently involve in AD pathology and cognitive deficit. In the present study, we have explored the neuroprotective potential of Fingolimod (FTY720), against Aluminium Chloride (AlCl3) induced experimental dementia in the rats.MethodAlCl3 at the dose of (175mg/kg, p.o.) daily on first to 35th day. Spatial and non‐spatial memory was evaluated by using Morris water maze and object recognition test. Fingolimod (0.25 and 0.5 mg/kg, p.o.) was administered at weekly intervals after administered AlCl3 in rats. Administered AlCl3 in rats produced cognitive deficit and caused significant elevation in markers and oxidative stress and degenerative changes in hippocampus and cortical brain region.ResultOn the countatary, fingolimod treatment attenuate AlCl3 induced cognitive decline, reduced oxidative burden and able to preserve neuronal architecture and prevent neuronal loss in hippocampus and cortical brain region of the rats.ConclusionThe present study suggests that Fingolimod (FTY 720) show beneficial effects in treating dementia. Our data demonstrated that Fingolimod could be effective in the protection of toxicity induced by Aluminium chloride
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.