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Dietary Chitosan Attenuates High-Fat Diet-Induced Oxidative Stress, Apoptosis, and Inflammation in Nile Tilapia (Oreochromis niloticus) through Regulation of Nrf2/Kaep1 and Bcl-2/Bax Pathways
by
, , , , and
Aya G. Rashwan
1,†,
Doaa H. Assar
2,†,
Abdallah S. Salah
3,4,
**aolu Liu
5,6,
Ibrahim I. Al-Hawary
1,
Mohammed H. Abu-Alghayth
7,
Shimaa M. R. Salem
8,
Karim Khalil
9,
Nemany A. N. Hanafy
10, 
Alaa Abdelatty
11,
Luyang Sun
5,6,* and
Zizy I. Elbialy
1,* 
1
Department of Fish Processing and Biotechnology, Faculty of Aquatic and Fisheries Sciences, Kafrelsheikh University, Kafrelsheikh 33516, Egypt
2
Clinical Pathology Department, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh 33516, Egypt
3
Department of Aquaculture, Faculty of Aquatic and Fisheries Sciences, Kafrelsheikh University, Kafrelsheikh 33516, Egypt
4
Institute of Aquaculture, Faculty of Natural Sciences, University of Stirling, Stirling FK9 4LA, UK
5
Single-Cell Center, Shandong Key Laboratory of Energy Genetics and Shandong Energy Institute, Qingdao Institute of Bioenergy and Bioprocess Technology, CAS Key Laboratory of Biofuels, Chinese Academy of Sciences, Qingdao 266101, China
6
University of Chinese Academy of Sciences, Bei**g 101408, China
7
Department of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, P.O. Box 255, Bisha 67714, Saudi Arabia
8
Department of Animal Nutrition and Nutritional Deficiency Diseases, Faculty of Veterinary Medicine, Mansoura University, Mansoura 33516, Egypt
9
Department of Veterinary Medicine, College of Applied & Health Sciences, A’Sharqiyah University, P.O. Box 42, 400 Ibra, Oman
10
Group of Molecular Cell Biology and Bionanotechnology, Nanomedicine Department Institute of Nanoscience and Nanotechnology, Kafrelsheikh University, Kafrelsheikh 33516, Egypt
11
Pathology Department, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh 33516, Egypt
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Biology 2024, 13(7), 486; https://doi.org/10.3390/biology13070486
Submission received: 30 May 2024
/
Revised: 20 June 2024
/
Accepted: 21 June 2024
/
Published: 30 June 2024
(This article belongs to the Section Biochemistry and Molecular Biology)
Simple Summary
Fatty liver injury is common in farmed fish, but its molecular mechanisms are not well understood. An eight-week feeding trial was conducted to investigate the effects of dietary chitosan on high-fat diet (HFD)-induced liver damage in Nile tilapia. Six diets with varying fat and chitosan levels were tested. Fish on the HFD showed increased growth, fat accumulation, elevated liver injury markers, and higher levels of pro-apoptotic and inflammatory markers. Chitosan supplementation mitigated these effects and reduced intestinal injury by improving antioxidant defense and reducing inflammation and apoptosis through the nrf2 and cox2 pathways.
Abstract
Fatty liver injury is a prevalent condition in most farmed fish, yet the molecular mechanisms underpinning this pathology remain largely elusive. A comprehensive feeding trial spanning eight weeks was conducted to discern the potential of dietary chitosan in mitigating the deleterious effects of a high-fat diet (HFD) while concurrently exploring the underlying mechanism. Growth performance, haemato-biochemical capacity, antioxidant capacity, apoptotic/anti-apoptotic gene expression, inflammatory gene expression, and histopathological changes in the liver, kidney, and intestine were meticulously assessed in Nile tilapia. Six experimental diets were formulated with varying concentrations of chitosan. The first three groups were administered a diet comprising 6% fat with chitosan concentrations of 0%, 5%, and 10% and were designated as F6Ch0, F6Ch5, and F6Ch10, respectively. Conversely, the fourth, fifth, and sixth groups were fed a diet containing 12% fat with chitosan concentrations of 0%, 5%, and 10%, respectively, for 60 days and were termed F12Ch0, F12Ch5, and F12Ch10. The results showed that fish fed an HFD demonstrated enhanced growth rates and a significant accumulation of fat in the perivisceral tissue, accompanied by markedly elevated serum hepatic injury biomarkers and serum lipid levels, along with upregulation of pro-apoptotic and inflammatory markers. In stark contrast, the expression levels of nrf2, sod, gpx, and bcl-2 were notably decreased when compared with the control normal fat group. These observations were accompanied by marked diffuse hepatic steatosis, diffuse tubular damage, and shortened intestinal villi. Intriguingly, chitosan supplementation effectively mitigated the aforementioned findings and alleviated intestinal injury by upregulating the expression of tight junction-related genes. It could be concluded that dietary chitosan alleviates the adverse impacts of an HFD on the liver, kidney, and intestine by modulating the impaired antioxidant defense system, inflammation, and apoptosis through the variation in nrf2 and cox2 signaling pathways.
Keywords:
chitosan; high-fat diet; apoptosis; oxidative stress; nrf2/kaep1; bcl-2/bax
