chrysin and Cadmium-Poisoning

This study aimed to determine the potential protective effects of chrysin (CHR) on experimental cadmium (Cd)-induced lung toxicity in rats. To this end, rats were divided into five groups; Control, CHR, Cd, Cd + CHR25, Cd + CHR50. In the study, rats were treated with CHR (oral gavage, 25 mg/kg and 50 mg/kg) 30 min after giving Cd (oral gavage, 25 mg/kg) for 7 consecutive days. The effects of Cd and CHR treatments on oxidative stress, inflammatory response, ER stress, apoptosis and tissue damage in rat lung tissues were determined by biochemical and histological methods. Our results revealed that CHR therapy for Cd-administered rats could significantly reduce MDA levels in lung tissue while significantly increasing the activity of antioxidant enzymes (SOD, CAT, GPx) and GSH levels. CHR agent exerted antiinflammatory effect by lowering elevated levels of NF-κB, IL-1β IL-6, TNF-α, RAGE and NRLP3 in Cd-induced lung tissue. Moreover CHR down-regulated Cd-induced ER stress markers (PERK, IRE1, ATF6, CHOP, and GRP78) and apoptosis markers (Caspase-3, Bax) lung tissue. CHR up-regulated the Bcl-2 gene, an anti-apoptotic marker. Besides, CHR attenuated the side effects caused by Cd by modulating histopathological changes such as hemorrhage, inflammatory cell infiltration, thickening of the alveolar wall and collagen increase. Immunohistochemically, NF-κB and Caspase-3 expressions were intense in the Cd group, while these expressions were decreased in the Cd + CHR groups. These results suggest that CHR exhibits protective effects against Cd-induced lung toxicity in rats by ameliorating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and histological changes.

Topics: Animals; Antioxidants; Apoptosis; Biomarkers; Cadmium; Cadmium Poisoning; Caspase 3; Endoplasmic Reticulum Stress; Lung; NF-kappa B; Oxidative Stress; Rats

In this study, chrysin as a natural flavonoid was encapsulated in nanoliposomal structures, and the synthesized nanoliposome-loaded chrysin (NLC) was further characterized for its physical properties and cytoprotective effects in mice that received cadmium-containing water. The results showed that the synthesized NLC is possessed spherical structure with the size of 185.1 nm and negative surface charge of - 26 mV with a poly dispersity index of 0.26. The mice received cadmium (2 mg/kg body weight/day) through drinking water showed weight loss and decease in the feed intake significantly (p ≤ 0.05). The cadmium notably (p ≤ 0.05) increased the liver enzymes including aspartate aminotransferase, alanine transaminase, and alkaline phosphatase; altered the liver metal deposition (cadmium, copper, manganese, selenium, and zinc); and induced hepatic oxidative stress (inducible nitric oxide synthase, catalase, superoxide dismutase, and glutathione peroxidase genes) with no remarkable histopathological changes. Furthermore, the cadmium impaired the morphology of jejunum through reducing villus height and villus width and increasing the crypt depth. Providing NLC as a dietary supplement at the concentrations of 2.5 and 5 mg/kg mice body weight significantly (p ≤ 0.05) improved the feed intake and body weight gain, modulated the liver enzymes, and alleviated the hepatic oxidative stress. The NLC also improved the antioxidant mineral deposition in the liver and morphohistological structure of jejunum. Consequently, the NLC is suggested as a potential dietary supplement to alleviate the symptoms of cadmium-induced toxicity in mice.

Topics: Animals; Antioxidants; Cadmium; Cadmium Poisoning; Catalase; Flavonoids; Glutathione Peroxidase; Liver; Mice; Oxidative Stress; Superoxide Dismutase