**Background**
Glucocorticoids are a class of steroid hormones that play a pivotal role in regulating immune responses and maintaining homeostasis. In particular, the modulation of the Notch signaling pathway has emerged as a critical mechanism for treating various autoimmune and inflammatory conditions. Dysregulation of this pathway can lead to an imbalance in T-cell subsets, contributing to diseases such as autoimmune uveitis, or impact cognitive functions through the modulation of synaptic plasticity in the hippocampus. Understanding the interplay between glucocorticoid activity and Notch signaling is essential for developing targeted therapies for immune-mediated disorders and neurological impairments. In this context, we will introduce a potent glucocorticoid and orally active Notch inhibitor – Prednisone.
**Definition**
Prednisone (specifically Prednisone acetate) is a glucocorticoid and orally active Notch inhibitor with a molecular weight of 400.46 and the chemical formula C23H28O6. It targets IL-17, IL-10, and IL-4 to modulate immune responses.
**In Vivo Studies**
The Prednisone biological activity has been extensively evaluated in various animal models to determine its effects on the immune system and cognitive function. In a study involving C57BL/6 mice, Prednisone acetate (5 mg/kg; intragastric gavage; once daily for 4 weeks) was used to induce hippocampal long-term potentiation (LTP) impairment. The results showed that the treatment caused neuronal lesions in the dentate gyrus, reduced the levels of glutamic acid (Glu) and gamma-aminobutyric acid (GABA), and decreased the expression of N-methyl-D-aspartate receptors (NMDAR2A) in the hippocampus. This led to a significant reduction in population spikes after high-frequency stimulation and impaired spatial memory, as evidenced by reduced crossing times compared to the control group.
Furthermore, Prednisone in vivo studies in rats with experimental autoimmune uveitis (EAU) demonstrated its anti-inflammatory potential. Administration of Prednisone acetate (6 mg/kg; gavage; once daily for 15 days) reduced ocular and peripheral inflammatory responses. The compound bound with high affinity to the pocket of Notch signaling-related molecules, inhibiting Notch activation and restoring Th1/Th2 and Th17/Treg immune homeostasis by decreasing Th1 and Th17 frequencies while increasing Th2 and Treg frequencies. According to the Prednisone technical information, these results highlight its dual role in modulating both neurological plasticity and systemic inflammation. In conclusion, Prednisone is a versatile glucocorticoid that acts as a Notch inhibitor to regulate immune homeostasis and influence hippocampal function.
Keywords
Prednisone, 125-10-0, Prednisone 21-acetate, Glucocorticoid Receptor, Interleukin Related, Notch, IL, Hippocampus, Experimental autoimmune uveitis, Inhibitor, inhibitor, inhibit
References
[1] Prednisolone acetate
[2] Wang Y, et al. Intragastric administration of prednisone acetate induced impairment of hippocampal long-term potentiation [J]. Brain Research, 2023, 1805: 148270.
[3] Zhou M, Qu R, Yin X, et al. Prednisone acetate modulates Th1/Th2 and Th17/Treg cell homeostasis in experimental autoimmune uveitis via orchestrating the Notch signaling pathway [J]. International Immunopharmacology, 2023, 116: 109809.