Sibering, Bianca (2018) Cyclosporin: A double edged sword. Bachelor's Thesis, Life Science and Technology.
|
Text
final thesis Bianca.pdf Download (354kB) | Preview |
|
![[img]](https://fse.studenttheses.ub.rug.nl/style/images/fileicons/text.png) |
Text
toestemming.pdf Restricted to Registered users only Download (94kB) |
Abstract
Since cyclosporin was successfully tested to prevent graft rejection in 1978 the field of organ transplants became increasingly important. Cyclosporin works as an immunosuppressant by reducing T-cell function. Multiple studies have shown that cyclosporin also has a protective effect on kidneys against ischemia injury and that this positive effect is concentration dependent. When cyclosporin is used in high concentrations it has a nephrotoxic effect. In this thesis we will explain how ischemia injury is caused and determine how the protective effect and the toxic effect are caused by cyclosporin. We will examine via which pathways this is caused and why it is a concentration dependent process. Cyclosporin causes nephrotoxicity via an imbalance between vasodilation and vasoconstriction. Cyclosporin leads to a protective effect against ischemia-reperfusion injury (IRI) by binding to cyclophilin D with peptidyl prolyl cis trans isomerase activity and eventually blocking the mPTPs (mitochondrial Permeability Transition Pores). The toxic and protective effect are caused via 2 different mechanisms and is concentration dependent because of the high affinity of cyclosporin for cyclophilin D. Together with other protective compounds cyclosporin could be a successful drug against IRI.
| Item Type: | Thesis (Bachelor's Thesis) |
|---|---|
| Supervisor name: | Graaf, I.A.M. de |
| Degree programme: | Life Science and Technology |
| Thesis type: | Bachelor's Thesis |
| Language: | English |
| Date Deposited: | 13 Jul 2018 |
| Last Modified: | 20 Jul 2018 11:38 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/17855 |
Actions (login required)
 |
View Item |