The Roles of Bita-Adrenergic Receptor Blockers in Interstitial Cystitis

Interstitial cystitis (IC) is a debilitating disease characterized by chronic inflammation of the urinary bladder. β-Adrenergic receptor blockers appear to have a beneficial clinical effect in IC. In this paper, we review the evidence of an association between β- adrenergic receptor blockade and IC. The information was obtained from MEDLINE. Genetic studies have provided the opportunity to determine which proteins link β- adrenergic receptor blockade to IC pathology. In particular, this link involves the major histocompatibility complex class II molecules, the renin-angiotensin system, the transcription factor nuclear factor-κB, the nerve growth factor, and the vascular endothelial growth factor. Β-Adrenergic receptor blockers also exert anti-IC effects through non-genomic factors, including stress, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase-2, oxidative stress, and nitric oxide synthase. In conclusion, β-adrenergic receptor blockade may play a beneficial role in IC treatment. Additional investigations that examine β-adrenergic receptor blockers as IC therapeutics are required to further elucidate this role

The Beneficial Role of Vitamin D in Interstitial Cystitis

Interstitial cystitis (IC) is a poorly understood chronic bladder disorder that is generally characterized by bladder discomfort and increased urination urgency and frequency. Vitamin D levels are associated with bladder pathology, and both rat and human bladders express receptors for vitamin D3. Vitamin D significantly reduced edema and bladder wall leukocyte infiltration in a IC animal model. Genetic studies have provided the opportunity to determine which proteins link vitamin D to IC pathology (i.e., the major histocompatibility complex (MHC) class II molecules, the transcription factor nuclear factor kappa B (NF-κB), RANTES (regulated on activation, normal T cell expressed and secreted), epidermal growth factor (EGF), transforming growth factor beta (TGF-β) family, and vascular endothelial growth factor (VEGF)). Vitamin D also exerts its effect on IC through non-genomic factors, i.e., Bacillus Calmette-Guérin (BCG) vaccination, mast cells and histamine, prostaglandins (PGs), reactive oxygen species (ROS), and inducible nitric oxide synthase (iNOS). Conclusion: Vitamin D may have a beneficial role in IC. Calcitriol is best used for IC because it is the active form of the vitamin D3 metabolite, and it modulates inflammatory cytokine expression. Further investigation with calcitriol in IC patients is needed

The Role of Vitamin D in Primary Biliary Cirrhosis: Possible Genetic and Cell Signaling Mechanisms

Primary biliary cirrhosis (PBC) is an immune-mediated chronic inflammatory disease of the liver of unknown etiology. Vitamin D deficiency is highly prevalent in patients with PBC, and many studies have demonstrated the significant effect of calcitriol on liver cell physiology. Vitamin D has antiproliferative and antifibrotic effects on liver fibrosis. Genetic studies have provided an opportunity to determine which proteins link vitamin D to PBC pathology (e.g., the major histocompatibility complex class II molecules, the vitamin D receptor, toll-like receptors, apolipoprotein E, Nramp1, and cytotoxic T lymphocyte antigen-4). Vitamin D also exerts its effect on PBC through cell signaling mechanisms, that is, matrix metalloproteinases, prostaglandins, reactive oxygen species, and the transforming growth factor betas. In conclusion, vitamin D may have a beneficial role in the treatment of PBC. The best form of vitamin D for use in the PBC is calcitriol because it is the active form of vitamin metabolite, and its receptors are present in the sinusoidal endothelial cells, Kupffer cells, and stellate cells of normal livers, as well as in the biliary cell line

Beneficial role of vitamin D in the prevention of certain respiratory diseases

There is evidence of aberrations in the vitamin D–endocrine system in subjects with respiratory diseases. Vitamin D deficiency is highly prevalent in patients with respiratory diseases, and patients who receive vitamin D have significantly larger improvements in inspiratory muscle strength and maximal oxygen uptake. Studies have provided an opportunity to determine which proteins link vitamin D to respiratory pathology, including the major histocompatibility complex class II molecules, vitamin D receptor, vitamin D-binding protein, chromosome P 450 , Toll-like receptors, poly(ADP-ribose) polymerase-1, and the reduced form of nicotinamide adenine dinucleotide phosphate. Vitamin D also exerts its effect on respiratory diseases through cell signaling mechanisms, including matrix metalloproteinases, mitogen-activated protein kinase pathways, the Wnt/β-catenin signaling pathway, prostaglandins, reactive oxygen species, and nitric oxide synthase. In conclusion, vitamin D plays a significant role in respiratory diseases. The best form of vitamin D for use in the treatment of respiratory diseases is calcitriol because it is the active metabolite of vitamin D 3 and modulates inflammatory cytokine expression. Further investigation of calcitriol in respiratory diseases is needed