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Catechins, phenolic compounds renowned for their superior antioxidant and metal chelating attributes, are commonly found in foods. Cadmium (Cd) is a highly toxic heavy metal especially detrimental to the liver. However, the potential toxicologic effects of catechins against Cd-induced hepatotoxicity remains poorly studied. To investigate the preventive effects of catechins on Cd exposure, adult C57/BL6J mice were employed, receiving 100 mg/kg body weight (BW) catechins for consecutive 14 days by gavage, followed by acute exposure to 20 mg/ kg BW Cd on the final day. Focusing on the liver, our findings demonstrated that catechins effectively alleviated Cd-induced hepatoxicity, including the hepatic Cd accumulation, transaminases levels in serum, inflammation and oxidative stress in the liver. By using brusatol, a Nrf2 inhibitor, the prevention of catechins was reversed, highlighting the crucial key to Kelch-like ECH-associated protein 1 (Keap1)- Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in counteracting Cd-induced hepatoxicity. Our results revealed the beneficial effect of catechins on alleviating Cd-induced hepatotoxicity through the Keap1-Nrf2 pathway, and also provided a novel insight into the beneficial properties of catechins to counteract metal toxicity。The liver serves as the primary target organ for Cd toxicity. The impacts of catechins and Cd on hepatotoxicity were visualized clearly with H&E staining. The images of Control group presented plump, 

healthy, and natural liver cells. Conversely, the hepatocytes in the Cd group exhibited somewhat loosely arranged and obvious inflammatory infiltration. Upon intervention with catechins, the inflammatory infiltration of hepatocytes was alleviated, restoring a morphology more akin to that of the Control group (Fig. 2A). Furthermore, the levels of transaminases in serum, including AST, ALT and its ratio, were also measured to reflect the fundamental liver function. Following Cd exposure, there were significant increases in both AST and ALT levels in the Cd group, while the AST/ALT ratio dropped to a lower level than that in the Control group, indicating impaired liver function. In marked contrast, pre-exposure to catechins exerted an obvious protective effect, significantly reducing serum AST and ALT levels and restoring their ratio to a level more closely aligned with that in the Control group (Fig. 2B–D). Inflammation typically serves as the marker indicating the severity of acute injury (Chen et al., 2018). In the Cd group, there was a notable decrease in the levels of the anti-inflammatory cytokine IL-10, while the。proinflammatory cytokines TNF-α and IL-1β went up distinctly. However, the prevention of catechins led to a restoration of these protein levels, which closely resembled those in the Control group (Fig. 2E–G). A consistent trend was observed in the expression of genes related to inflammation. Treated with Cd, there was a noticeable upregulation in the expression levels of proinflammatory cytokines, particularly a substantial upregulation of TNF-α compared with the Control group. Conversely, pre-treatment with catechins mitigated these inflammatoryresponses, resulting in reduced inflammatory levels in the Cat + Cd group (Fig. 2H).

293 [HEK-293] (人胚腎細胞) 
5637 (人膀胱癌細胞) 
293A (人胚腎細胞) 
22RV1 (人前列腺癌細胞) 
293T [HEK-293T](人胚腎細胞) 
3T3-L1 (小鼠胚胎成纖維細胞)
4T1 (小鼠乳腺癌細胞) 
6T-CEM (人T細胞白血病細胞) 
769-P (人腎細胞腺癌細胞) 
786-O [786-0] (人腎透明細胞腺癌細胞) 
95-D [PLA-801D] (人高轉移肺癌細胞) 
A172 (人膠質母細胞瘤細胞) 
A2780 (人卵巢癌細胞)
A-375 (人惡性黑色素瘤細胞) 
A-431 (人表皮癌細胞) 
A549 [A-549] (人非小細胞肺癌細胞) 
A-673 (人橫紋肌肉瘤細胞) 
A9 (小鼠皮下結締組織細胞)
AAV-293 (人胚腎細胞) 
Acc-2 (人涎腺腺樣囊性癌細胞)
ACHN (人腎細胞腺癌細胞) 
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Ana-1 (小鼠巨噬細胞)
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AR42J (大鼠胰腺外分泌細胞)
ARPE-19 (人視網膜上皮細胞) 
AsPC-1 (人轉移胰腺腺癌細胞) 
AtT-20 (小鼠垂體瘤細胞)
B16 (小鼠黑色素瘤細胞)
Bcap-37 (人乳腺癌細胞)
BEL-7402 (人肝癌細胞)
BEL-7404 (人肝癌細胞)