Citrus flavanones prevent systemic inflammation and ameliorate oxidative stress in C57BL/6J mice fed high-fat diet

Abstract

The flavanones hesperidin, eriocitrin and eriodictyol were investigated for their prevention of the oxidative stress and systemic inflammation caused by high-fat diet in C57BL/6J mice. The mice received a standard diet (9.5% kcal from fat), high-fat diet (45% kcal from fat) or high-fat diet supplemented with hesperidin, eriocitrin or eriodictyol for a period of four weeks. Hesperidin, eriocitrin and eriodictyol increased the serum total antioxidant capacity, and restrained the elevation of interleukin-6 (IL-6), macrophage chemoattractant protein-1 (MCP-1), and C-reactive protein (hs-CRP). In addition, the liver TBARS levels and spleen mass (g per kg body weight) were lower for the flavanone-treated mice than in the unsupplemented mice. Eriocitrin and eriodictyol reduced TBARS levels in the blood serum, and hesperidin and eriodictyol also reduced fat accumulation and liver damage. The results showed that hesperidin, eriocitrin and eriodictyol had protective effects against inflammation and oxidative stress caused by high-fat diet in mice, and may therefore prevent metabolic alterations associated with the development of cardiovascular diseases in other animals.

Effectiveness of Eriomin® in managing hyperglycemia and reversal of prediabetes condition: A double‐blind, randomized, controlled study

“…In the present study, Eriomin supplementation resulted in improved blood serum antioxidant status and reduced oxidative stress, evidenced by increased antioxidant capacity (+6%) associated with reduced lipid peroxidation marker (−17%). Our results are consistent with previous studies, which observed a reduction of lipid peroxidation on the blood serum, liver, and kidneys of diabetic rats treated with eriocitrin (Bucolo et al, ; Ferreira et al, ; Miyake, Yamamoto, Tsujihara, & Osawa, ). In addition, eriodictyol protected against kidney injury through activating nuclear factor‐erythroid related factor 2 (Nrf2; Li et al, ).…”

“…These results suggest absence or nondetectable toxicity or impairment of liver function, as previously shown of lemon flavonoid supplementation (Hiramitsu et al, ). In addition, a study with mice showed that eriocitrin protected against liver damage caused by consumption of the high‐fat diet (Ferreira et al, ).…”

Eriodictyol inhibits high glucose‐induced oxidative stress and inflammation in retinal ganglial cells

“…10,18 Li et al 10 reported that eriodictyol elevated the activities of SOD, CAT, and GPx, as well as inhibited the production of malondialdehyde, thiobarbituric acid reactive substances (TBARS), TNF-α and IL-1β in kidney tissues. 10,18 Li et al 10 reported that eriodictyol elevated the activities of SOD, CAT, and GPx, as well as inhibited the production of malondialdehyde, thiobarbituric acid reactive substances (TBARS), TNF-α and IL-1β in kidney tissues.…”

Gold-quercetin nanoparticles prevent metabolic endotoxemia-induced kidney injury by regulating TLR4/NF-kB signaling and Nrf2 pathway in high fat diet fed mice

“…Recent studies have further demonstrated that HFD could affect the peripheral tissues, as well as cause systematic inflammation by directly or indirectly activating Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kB) pathway. 11,12 Of note, on one hand, biomechanical experiments and clinical observations have illustrated that long-term intake of HFD results in lipid accumulation and endotoxemia, which can cause increase in inflammatory cytokines in the serum and organs and inflammationrelated signaling activation, promoting the development of nonalcoholic fatty liver disease (NAFLD) and systemic disorder. 11,[13][14][15] On the other hand, HFD significantly increases the production of reactive oxygen species (ROS), which further release superoxide anion and cause oxidative stress in the kidney by stimulating podocyte injury.…”

“…11,12 Of note, on one hand, biomechanical experiments and clinical observations have illustrated that long-term intake of HFD results in lipid accumulation and endotoxemia, which can cause increase in inflammatory cytokines in the serum and organs and inflammationrelated signaling activation, promoting the development of nonalcoholic fatty liver disease (NAFLD) and systemic disorder. 11,[13][14][15] On the other hand, HFD significantly increases the production of reactive oxygen species (ROS), which further release superoxide anion and cause oxidative stress in the kidney by stimulating podocyte injury. [15][16][17] Hence, antioxidant therapy may be involved in the pathological process of kidney injury.…”