Baicalein ameliorates cadmium-induced hepatic and renal oxidative damage in rats

Wang, Jicang; Zhu, Huali; Cai, Zaisheng; Wang, Hongwei; Zhou, Yang

doi:10.18805/ijar.b-853

Cited by 9 publications

(8 citation statements)

References 21 publications

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“…As shown in Table 2, the body weight of Cd-induced rats was significantly reduced compared with that of rats in the control group. These results are consistent with those of a previous study (Wang et al 2019). The weight loss of rats may be due to the damage in the intestinal mucosa and the disorder of glucocorticoid system caused by Cd.…”

Section: Effect Of Nar On Caspase-9 and -3 Mrna Expressionsupporting

confidence: 93%

Protective Effect of Naringenin on Cadmium-induced Toxicity in Rat Liver

Wang

Ding

Kou

et al. 2021

IJAR

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Background: Cadmium (Cd) is a widespread environmental toxic heavy metal. Naringin (Nar) is reported to have a protective effect on Cd-induced liver injury. This study aimed to explore the hepatic injury induced by Cd and the protective effects of Nar on Cd-induced oxidative stress and apoptosis in rat liver. Methods: In accordance with groups, male SD rats were injected intraperitoneally with Cd and orally with Nar every day. The treatment period was 3 weeks. Body weight, the morphological changes in liver, the activity of antioxidant indices and expression of the apoptotic genes caspase-3 and -9 were assessed. Result: Results showed that the body weight of Cd-exposed rats decreased, the superoxide dismutase and catalase activities in liver decreased, the glutathione content decreased and the malondialdehyde content increased. Further, Cd-induced hepatic structural damage and cell apoptosis were observed. However, Nar could alleviate liver damage caused by Cd. Therefore, Cd caused oxidative damage and cell apoptosis in rat liver, while Nar had preventive and ameliorative effects on these injuries.

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Section: Effect Of Nar On Caspase-9 and -3 Mrna Expressionsupporting

confidence: 93%

Protective Effect of Naringenin on Cadmium-induced Toxicity in Rat Liver

Wang

Ding

Kou

et al. 2021

IJAR

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“…GSH acts as a major endogenous antioxidant with respect to the gut, GPX transforms GSH to its GSSG oxidized type. Oxidative stress will increase the GSSG level along with a corresponding decrease in SOD, GPX, and GSH concentrations [ 49 , 50 ]. Therefore, we believe that dietary inclusion of GOx has been shown to improve blood profile glucose and SOD of lactating sows by enhancing the immune system.…”

Section: Resultsmentioning

confidence: 99%

Dietary inclusion of glucose oxidase supplementation to corn-wheat-based diet enhance growth performance, nutrient digestibility, blood profile of lactating sows

Shanmugam¹,

Liu²,

Chen³

et al. 2021

J Anim Sci Technol

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“…It is difficult for animals and humans to excrete Cd as it can be present in the body for as long as 30 years ( Nordberg, 2009 ). Previous studies have shown that the liver and kidney are the two main target organs of Cd toxicity and that the degree of damage to the liver is far higher than that of the kidney, and cadmium can even cause liver cancer ( Song et al, 2016 ; Liu et al, 2017a ; Wang et al, 2017 ; Wang et al, 2018 ; Gong et al, 2019 ; Wang et al, 2019 ). The amount that Cd stored in the liver is approximately one third of the total amount of the whole body ( Marettova et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Gap Junction Intercellular Communication Negatively Regulates Cadmium-Induced Autophagy and Inhibition of Autophagic Flux in Buffalo Rat Liver 3A Cells

et al. 2020

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Cadmium is an important environmental pollutant that poses a serious threat to the health of humans and animals. A large number of studies have shown that the liver is one of the important target organs of cadmium. Stimulation of cells can lead to rapid changes in gap junction intercellular communication (GJIC) and autophagy. Previous studies have shown that cadmium can inhibit GJIC and induce autophagy. In order to understand the dynamic changes of GJIC and autophagy in the process of cadmium-induced hepatotoxic injury and the effects of GJIC on autophagy, a time-gradient model of cadmium cytotoxicity was established. The results showed that within 24 h of cadmium exposure, 5 μmol/L cadmium inhibited GJIC by down regulating the expression levels of connexin 43 (Cx43) and disturbing the localization of Cx43 in Buffalo rat liver 3A (BRL 3A) cells. In addition, cadmium induced autophagy and then inhibited autophagic flux in the later stage. During this process, inhibiting of GJIC could exacerbate the cytotoxic damage of cadmium and induce autophagy, but further blocked autophagic flux, promoting GJIC in order to obtain the opposite results.

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Baicalein ameliorates cadmium-induced hepatic and renal oxidative damage in rats

Cited by 9 publications

References 21 publications

Protective Effect of Naringenin on Cadmium-induced Toxicity in Rat Liver

Protective Effect of Naringenin on Cadmium-induced Toxicity in Rat Liver

Dietary inclusion of glucose oxidase supplementation to corn-wheat-based diet enhance growth performance, nutrient digestibility, blood profile of lactating sows

Gap Junction Intercellular Communication Negatively Regulates Cadmium-Induced Autophagy and Inhibition of Autophagic Flux in Buffalo Rat Liver 3A Cells

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