Investigation of the ameliorative effects of baicalin against arsenic trioxide-induced cardiac toxicity in mice

Iron overload promotes intervertebral disc degeneration via inducing oxidative stress and ferroptosis in endplate chondrocytes.

Simple Summary Deoxynivalenol (DON)-contaminated feed may cause anorexia, vomiting, immunosuppression, and intestinal dysfunction in pigs, which would lead to growth retardation and great losses in the pig industry. In this study, the effects of resveratrol (RES) on growth performance, the intestinal barrier, antioxidant capacity, and mitochondrial function in weaned pigs fed with DON-contaminated diets were investigated. Dietary supplementation with resveratrol increased the average daily feed intake of piglets. Diets supplemented with resveratrol increased the villus height and the ratio of the jejunum villus height to crypt depth, increased the activities of superoxide dismutase (SOD), and increased the total antioxidant capacity in the jejunum mucosa. After being supplemented with RES, the level of reactive oxygen species (ROS) in mitochondria was decreased, while the mitochondrial membrane potential in the jejunum was increased. In conclusion, these results suggested that resveratrol effectively relieved DON-induced oxidative stress in weaned piglets, improved intestinal barrier function, enhanced mitochondrial function, and improved the growth performance of piglets. Abstract This study aimed to investigate the potential effects of resveratrol (RES) on intestinal function and oxidative stress in deoxynivalenol (DON)-challenged piglets. Twenty-four healthy Duroc × Yorkshire × Landrace weaned piglets at the age of 28 ± 1 days were randomly divided into four groups with six repetitions per group. The four groups were as follows: the control group (CON), fed with a basic diet; the RES group, fed with a basal diet + 300 mg/kg RES; the DON group, fed with a basal diet containing 2.65 mg/kg DON; and the DON + RES group, fed with a basal diet containing 2.65 mg/kg DON + 300 mg/kg RES. The results showed that the growth performance and intestinal function of DON-challenged piglets were significantly decreased (p < 0.05). Compared with the DON group, the average daily feed intake of piglets in the DON + RES group was significantly increased (p < 0.05). Additionally, dietary RES ameliorated DON-induced intestinal morphology impairment, as indicated by the increased (p < 0.05) jejunal villi height and the ratio of the jejunal villi height/crypt depth. Furthermore, after the addition of RES, the activities of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) in the jejunum mucosa were significantly increased, and the content of malondialdehyde (MDA) was significantly declined (p < 0.05). In addition, the level of reactive oxygen species (ROS) in the mitochondria was significantly reduced by RES, while the mitochondrial membrane potential in jejunum was significantly increased by RES (p < 0.05). However, there was no obvious difference between DON + RES and DON groups on average daily gain and the ratio of feed togain, except for the significant inhibition of average daily feed intake (p < 0.05). In conclusion, RES could effectively alleviate the DON-induced oxidative stress on weaned piglets, and reduce the damage to mitochondria and intestinal morphology, so as to improve the growth performance of piglets.

/pdf/resveratrol-improves-intestinal-morphology-and-anti-3d9ieann.pdf

Resveratrol Improves Intestinal Morphology and Anti-Oxidation Ability in Deoxynivalenol-Challenged Piglets

Apigenin ameliorates di(2-ethylhexyl) phthalate-induced ferroptosis: The activation of glutathione peroxidase 4 and suppression of iron intake.

Background: Hesperidin (HES) is a flavonoid glycoside found in the tangerine peel and has antioxidant properties. Arsenic trioxide (ATO) is an anti-tumour drug; however, its serious cardiotoxicity limits its clinical application. In addition, the protection of HES against ATO-induced cardiotoxicity has not been explored.

Objective: The study aims to investigate and identify the underlying effect and mechanism of HES on ATO-induced cardiotoxicity.

Methods: Fifty mice were randomly assigned to five groups. Mice were orally given HES:100 or 300 mg/kg/day concurrently and given ATO intraperitoneal injections: 7.5 mg/kg/day for 1 week. Blood and heart tissues were collected for examination. Evaluated in serum was the levels of creatine kinase (CK), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI). In addition, evaluated in heart tissues were the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, cleaved-Caspase-3, p62, Kelch-like ECH-associated protein 1 (Keap1), and nuclear factor erythroid 2-related factor 2 (Nrf2). The heart tissues were also examined for histopathology and mitochondrial ultrastructure.

Results: Compared with the ATO group, the HES treatment groups reduced the levels of CK, LDH, cTnI, ROS, MDA, TNF-α, IL-6, Bax, Caspase-3, cleaved-Caspase-3 and Keap1 and enhanced the levels of SOD, GSH, CAT, Bcl-2, p62 and Nrf2.

Conclusions: The results demonstrate that HES protects against ATO-induced cardiotoxicity, through inhibiting oxidative stress, and subsequent inflammation and apoptosis. The underlying results are closely related to the regulation of the p62-Keap1-Nrf2 signalling pathway.

Peixin Le

Papers

The protective mechanism of resveratrol against hepatic injury induced by iron overload in mice.