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Reports of Biochemistry and Molecular Biology
rbmb.net
Basic Sciences
http://rbmb.net
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2322-3480
2322-3480
10.61882/rbmb
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Herniarin Alleviates Sodium Arsenite-Induced Liver Toxicity in Mice by Attenuation of Oxidative Stress and Inflammation
بیوشیمی
Biochemistry
مقالات اصلی
Original Article
<div class="WordSection1">
<div style="text-align: justify;"><span style="page:WordSection1"><span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span lang="EN-GB" style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.4pt">Background: </span></span></span></span></i></b><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt">Arsenic is a serious threat to human health. Long-term exposure to arsenic has been linked to various harmful health effects, including liver damage. The liver damage caused by arsenic is mainly due to inflammation and oxidative stress. This research was performed to investigate the hepatoprotective effects of herniarin (HER), a coumarin derivative found in many plants, against hepatotoxicity induced by sodium arsenite (SA).</span></span></span></span></span></span></span></span></span></span><br>
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<span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt">Methods:</span></span></span></span></i></b><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt"> To induce hepatotoxicity, SA at a dose of 10 mg/kg was administered to mice for 30 days. HER at doses of 10, 25, and 50 mg/kg was given to mice for 30 days before SA administration. After completing the study protocol, the animals were euthanized, and blood and liver samples were collected for biochemical assessments.</span></span></span></span></span></span></span></span></span></span><br>
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<span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt">Results:</span></span></span></span></i></b><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt"> The results showed that SA increased liver enzymes and causes tissue damage, as well as elevated oxidative substances such as substances reactive to thiobarbituric acid in the liver, while simultaneously leading to a decrease in total thiol reserves and decreases in antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. Western blot analysis showed decreased protein expression of Nrf2, NQO1, and HO-1.</span></span></span></span></span></span></span></span></span></span><br>
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<span style="font-size:10pt"><span style="text-justify:kashida"><span style="text-kashida:0%"><span style="line-height:normal"><span style="tab-stops:396.55pt"><span style="font-family:Calibri,sans-serif"><b><i><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt">Conclusions:</span></span></span></span></i></b><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black"><span style="letter-spacing:-.2pt"> Pretreatment with HER ameliorated SA-associated liver injury in mice. HER reduced hepatotoxicity and oxidative damage caused by SA and increased antioxidant factors.</span></span></span></span></span></span></span></span></span></span></span></div>
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Arsenic, Hepatotoxicity, Herniarin, Nrf2, Oxidative stress.
181
190
http://rbmb.net/browse.php?a_code=A-10-1293-2&slc_lang=en&sid=1
Faride
Alvandi
100319475328460022398
100319475328460022398
No
Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mehrnoush
Matin
100319475328460022399
100319475328460022399
No
Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Maryam
Salehcheh
100319475328460022400
100319475328460022400
No
Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, IranDepartment of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Layasadat
Khorsandi
100319475328460022401
100319475328460022401
No
Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mehrnoosh
Moosavi
mehrnoosh.moosavi59@gmail.com
100319475328460022402
100319475328460022402
Yes
Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.