Add like
Add dislike
Add to saved papers

Induced Lesion and Inhibited Ihh-PTHrP Signalling Pathway Activity in the Articular Cartilage of Rats Caused by T-2 toxin.

This study aims to investigate the role of Ihh-PTHrP signalling pathway in the articular cartilage injury of rats caused by T-2 toxin. Sixty male Wistar rats were randomly divided into four groups: group A, normal diet; group B, normal diet plus the dissolvent (0.9% sodium chloride sterile aqueous solution containing ethanol); group C, normal diet plus low T-2 toxin (0.1 mg/kg BW/day) and group D, normal diet plus high T-2 toxin (0.2 mg/kg BW/day) by intragastric administration daily for 4 weeks. Histological changes in articular cartilage were assessed by HE staining and scanning electron microscopy. The expression of Ihh and PTHrP in cartilage was assessed by immunohistochemistry. There is a significant difference in average weight gain between group A and group D P < 0.01, groups A and D P < 0.001, respectively. The result of scanning electron microscopy and HE staining showed that the damage of articular cartilage was much severe with the increase of T-2 toxin. Immunohistochemical analysis indicated that the expression of Ihh in group A and group B was higher than that of group C and group D (P < 0.05, < 0.01, respectively). However, the expression of PTHrP was lower in group A and group B than that of group C and group D (P < 0.001, < 0.001, respectively). These results indicated that T-2 toxin can cause the damage to articular cartilage and weight loss in rats. The effect of T-2 toxin on articular cartilage of rat may be related to the Ihh-PTHrP pathway.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app