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Newer Agents for Topical Treatment
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Devinder Mohan Thappa, Malathi Munisamy
Prostaglandin F2 alpha (PGF2α) analogs: PGF2α analogs have been reported to be promising therapeutic options in vitiligo in both human and animal studies, with increased efficacy when combined with phototherapy or topical steroids. The therapeutic efficacy is mediated indirectly through induction of COX-2 and PGE2 and not due to direct effect on melanogenesis. Latanoprost (0.005%), Bimatoprost (0.03%), and Travoprost (0.004%) ophthalmic solutions are the PGF2α analogs that are being investigated in various studies [15–17].
Disorders of the respiratory system
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
Prostaglandin F2 alpha (Carboprost) should not be used in women with asthma because of the risk of bronchospasm. However, prostaglandin E1(Misoprostol) may be an option for treating postpartum haemorrhage in women with asthma because there is no evidence it worsens asthma29. Prostaglandin E1 or prostaglandin E2 can be considered for inducing labour in women with asthma because there is no evidence that they worsen asthma29.
Menstrual-Cycle-Related Disorders
Published in Jane M. Ussher, Joan C. Chrisler, Janette Perz, Routledge International Handbook of Women’s Sexual and Reproductive Health, 2019
Nancy Fugate Woods, Nancy J. Kenney
Over-production of uterine prostaglandins has been the most widely accepted etiologic explanation for dysmenorrhea (Dawood, 2006). Endometrial cells are sloughed during menstruation, and their disintegration releases arachidonic acid, which is a precursor for prostaglandin synthesis. In turn, prostaglandins stimulate myometrial hyper-contractility, which produces ischemia and hypoxic effects in the myometrium that induce pain. Prostaglandin production can be stimulated by epinephrine, peptide and steroid hormones, mechanical stimulation, and tissue trauma. In women with dysmenorrhea, falling levels of progesterone prior to menses initiate a process by which endometrial lysosomes liberate arachidonic acid, which, in turn, increases prostaglandin production. Women with dysmenorrhea have higher levels of prostaglandins in the luteal phase of their menstrual cycles than at other times and higher levels than do women without dysmenorrhea. PGF2-alpha (prostaglandin F2-alpha) has potent effects on vasoconstriction of the uterine blood vessels and enhances myometrial contraction. Although evidence supports contraction of an ischemic uterus as the cause of pain, it has also been suggested that prostaglandins sensitize nerve endings to pain (Iacovides et al., 2015). In addition, women with primary dysmenorrhea, as compared with women without, exhibit greater expression of genes that regulate pro-inflammatory cytokines and transform growth factor-beta, which are related to inflammation and may account for some of the symptoms women experience with dysmenorrhea (Iacovides et al., 2015).
Stanniocalcin-1 Reduced Intraocular Pressure in Two Models of Ocular Hypertension
Published in Current Eye Research, 2021
Gavin W. Roddy, Uttio Roy Chowdhury, Kjersten J. Monson, Michael P. Fautsch
Glaucomatous optic neuropathy (GON) remains the world’s leading cause of irreversible blindness.1 Currently, the only reliable therapeutic target is the reduction of intraocular pressure (IOP) by means of pharmacologic, laser, or surgical intervention. Of these, topical eye drop monotherapy is generally the initial treatment of choice for patients with GON or ocular hypertension2 of the available medication classes, Prostaglandin F2 alpha analogues (PGF2α) such as latanoprost are often used as first-line therapy3 given their low systemic side-effect profile, once daily dosing, and greater IOP-lowering effects compared to other classes of medications.4–6 However, up to 20% of patients have a diminished response to PGF2α analogues which has been associated with single polymorphisms in the prostaglandin F (FP) receptor.7–12 Additionally, patients can also be intolerant of the medication due to ocular side-effects including conjunctival hyperemia, surface irritation, pigmentation of the iris and periocular skin, orbital fat atrophy, hypertrichosis,13 intraocular inflammation,14,15 reactivation of herpes simplex keratitis and macular edema.16
Experimental drugs for the inhibition of preterm labor
Published in Expert Opinion on Investigational Drugs, 2020
Tegan Triggs, Sailesh Kumar, Murray Mitchell
The NF-κB complex is usually inactivated and bound to IκB-α (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha). This prevents it from activating transcription of pro-inflammatory cytokines. To initiate the cascade that involves freeing NF-κB from inhibition, TAK1 phosphorylates and activates the IκB kinase (IKK) complex. This complex consists of a regulatory subunit, IKKγ (also known as NF-κB essential modulator or NEMO), and two catalytic subunits IKKß and IKKα. Once activated, these catalytic subunits phosphorylate IκB-α. This targets it for degradation, freeing NF-κB subunits to translocate to the nucleus of the inflammatory cell to induce the expression of pro-inflammatory cytokines, prostaglandins, and other compounds. These include interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin (IL-1ß), tumor necrosis factor-alpha (TNF-α), matrix metalloproteinases (MMPs), and cyclooxygenase-2 (COX-2). Via the arachidonic acid pathway, other inflammatory compounds such as prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2α) [6] are also induced. TAK1 can also phosphorylate and activate MAPKs, which subsequently activates p38 MAPK. P38 MAPK is involved in intrauterine inflammation and labor onset, though the exact mechanism remains unclear [7].
Management of Citrus sinensis peels for protection and treatment against gastric ulcer induced by ethanol in rats
Published in Biomarkers, 2020
Asmaa Aboul Naser, Eman Younis, Amal El-Feky, Marwa Elbatanony, Manal Hamed
The previous study of Miller (1983) stated that prostaglandins affect various components of the mucosal defence pathways including maintaining blood flow, stimulating bicarbonate and mucus secretion, increasing the resistance of epithelial cells to injury and preventing leukocyte recruitment. In this study, ethanol consumption led to decrease PGE2 level that was consistent with the previous studies of Nartey et al. (2012) and Wang et al. (2015). The reactive oxygen species convert prostaglandin into 8-iso-prostaglandin F2alpha that causes vasoconstriction and platelet aggregation (Zhao et al. 2009, El-Maraghy et al. 2015). PGE2 also suppresses gastric circulation around the ulcerated mucosa and thus delays its healing effect (Hasgul et al. 2014).