From what does prednisolone protect rats? - briefly
Prednisolone safeguards rats against inflammation‑driven tissue damage and immune‑mediated injury, including endotoxin‑induced septic shock. It also reduces the severity of radiation‑induced organ injury.
From what does prednisolone protect rats? - in detail
Prednisolone confers protection to laboratory rats against a range of inflammatory and immune‑mediated challenges. In experimental models it reduces tissue damage caused by:
- Acute and chronic inflammation induced by lipopolysaccharide, carrageenan, or formalin injection.
- Autoimmune disorders such as experimental autoimmune encephalomyelitis and collagen‑induced arthritis.
- Oxidative stress generated by toxins like carbon tetrachloride, acetaminophen overdose, or heavy‑metal exposure.
- Radiation‑induced organ injury, particularly in lung and gastrointestinal tract.
- Sepsis‑related organ failure, where it dampens cytokine storms and stabilizes hemodynamics.
Mechanistically, prednisolone binds glucocorticoid receptors, translocates the complex to the nucleus, and modulates gene transcription. Up‑regulated anti‑inflammatory genes include annexin‑1, IL‑10, and IkBα, which inhibit NF‑κB signaling. Down‑regulated pro‑inflammatory mediators comprise TNF‑α, IL‑1β, IL‑6, COX‑2, and inducible nitric‑oxide synthase. The drug also suppresses leukocyte migration, reduces capillary permeability, and stabilizes lysosomal membranes, limiting cellular injury.
Pharmacokinetic data show peak plasma concentrations within 30–60 minutes after oral dosing, with a half‑life of 2–3 hours in rats. Effective protective doses range from 0.5 mg kg⁻¹ to 5 mg kg⁻¹, administered once daily or in divided doses, depending on the severity of the insult. Chronic administration requires monitoring for adrenal suppression, hyperglycemia, and bone demineralization, effects that can be mitigated by intermittent dosing schedules or co‑administration of mineralocorticoid‑sparing agents.
In summary, prednisolone shields rats from inflammatory, autoimmune, oxidative, radiative, and septic injuries through glucocorticoid receptor‑mediated transcriptional reprogramming, leukocyte modulation, and membrane stabilization. Proper dosing regimens maximize therapeutic benefit while minimizing adverse systemic effects.