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Ethnomedicinal and Pharmacological Importance of Glycyrrhiza glabra L
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Ashish K. Bhattarai, Sanjaya M. Dixit
Licorice causes the inhibition of 15-hydroxyprostaglandin dehydrogenase and delta13-prostaglandin reductase. 15-hydroxyprostaglandin dehydrogenase converts prostaglandins E2 and F2α to 15-ketoprostaglandins, which are inactive. This prevents the concentration of prostaglandin E2 and F2α towards degradation into inactive compounds (Baker 1994). Different prostaglandins have gastro shielding role. They help to maintain the mucosal integrity, and PGE2 is basically more important for this action. Increase in concentration of local prostaglandins promote the mucous secretion and cell proliferation in the stomach that ultimately promotes the healing of ulcers (Takeuchi and Amagase 2018).
Clinical Endocrinology of Pregnant Mares
Published in Juan Carlos Gardón, Katy Satué, Biotechnologies Applied to Animal Reproduction, 2020
PGs play an important role during delivery by promoting myometrial contractibility (PGF2α), along with oxytocin, and cervical ripening and relaxation (PGE2). Uteroplacental tissues are capable of synthesizing PGs and can be found in maternal plasma, fetal plasma, and allantoic fluid (Silver et al., 1979). However, its bioactivity is controlled by the enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), which converts the PGs into inactive metabolites, present in the maternal endometrium since approximately 150 days of pregnancy. In addition, the activity of this enzyme could be favored in the form of paracrine by P4 synthesized in the placenta (Han et al., 1995). On the other hand, the synthesis of PGs could be inhibited by P4, as described in pregnant sheep (Challis et al., 2000). Since the labile nature of PGs makes it difficult to measure one of these metabolites, 13,14-dihydro-15-keto-prostaglandin F-2α (PGFM) remained at low levels (<400 pg/mL) until day 200, then increased to peak pregnancy levels (>2000 pg/mL) by day 300 and remained at this value until parturition. PGFM uses one of its metabolites as an indicator of its circulating levels, with a term increase (2–4 ng/mL) being described, although it is during the second labor stage, when its value increases up to 50 times (Haluska and Currie, 1988; Vivrette et al. 2000) (Fig. 7.2).
Pathways of Arachidonic Acid Metabolism
Published in Murray D. Mitchell, Eicosanoids in Reproduction, 2020
The first step in the catabolism of prostaglandins is catalyzed by 15-hydroxyprostaglandin dehydrogenase (PGDH), which is a cytosolic enzyme. The 15-keto-derivatives so formed are substantially biologically inactive and are rapidly converted to the 13,14-dihydro-15-keto-derivatives that are the major circulating forms. A major site of such metabolism is the lung; almost all biologically active prostaglandins are metabolized during one passage through the lungs. Such metabolism occurs, first, by uptake into pulmonary cells and second, by the action of PGDH. Elimination of biologically active prostaglandins is completed by a series of beta oxidations and omega oxidation that result in the formation of a wide variety of products that are excreted in the urine. It should be noted that exceptions exist to the preceding description of prostaglandin catabolism. For instance, PGD2 is an extremely poor substrate for PGDH and prostacyclin may not be metabolized completely by the lungs since it is not a good substrate for the uptake mechanisms that transport prostaglandins into the pulmonary cells for subsequent metabolism.
Primary hypertrophic osteoarthropathy with severe arthralgia identified by gene mutation of SLCO2A1
Published in Modern Rheumatology Case Reports, 2021
Tatsuo Ishizuka, Kei Fujioka, Ichiro Mori, Tomofumi Takeda, Masayuki Fuwa, Takahide Ikeda, Koichiro Taguchi, Hiroyuki Morita, Kazuhiko Nakabayashi, Hironori Niizeki
Primary hypertrophic osteoarthropathy (PHO) or pachydermoperiostosis (PDP) was genetic disorder characterised by clubbed finger, hypertrophy of periostosis and the change of hypertrophic skin and 42 cases had been reported in Japan which was extremely predominant in male patients (Male: Female, 15:1). Mutated SLCO2A1 encoded prostaglandin E2 transport protein (HPDG) had been resulted in excessive PGE2 [1]. Firstly, Uppal et al. reported that mutations of HGPD genes which encodes 15-hydroxyprostaglandin dehydrogenase(15-PGDH) have been identified prostaglandin as the main causative factor of PDP [2,3]. Recent advances in the gene analysis of PDP patients focussed on mutation of solute carrier organic anion transport family member 2A1 (SLCO2A1) has been found in the 4 unrelated PDP patients [1].
The impact of circulating 25-hydroxyvitamin and oral cholecalciferol treatment on menstrual pain in dysmenorrheic patients
Published in Gynecological Endocrinology, 2019
Hatice Kucukceran, Ozhan Ozdemir, Serkan Kiral, Dilek Sensoz Berker, Rabia Kahveci, Adem Ozkara, Cemal Reşat Atalay, İhsan Ates
In addition to its role in the calcium metabolism, 1,25-dihydroxyvitamin-D3 (1,25(OH)2D3) has anti-proliferative/immunomodulatory activity in various tissues [4]. The 1-hydroxylase (1-OHase) enzyme, which is necessary for Vitamin-D receptors and 1,25(OH)2D3 synthesis, has a wide distribution in the body and has been found to be widely present in the endometrial tissue [4]. For this reason, Vitamin-D synthesis occurs in the human uterus and endometrium seems to be a target region for this vitamin [4]. Vitamin-D decreases prostaglandin production by causing decreased cyclooxygenase-2 expression in endometrium, increases prostaglandin inactivation by causing up-regulation in the 15-hydroxyprostaglandin dehydrogenase enzyme, and regulates prostaglandin receptor expression, thereby being effective in reducing menstrual pain [5,6].
Role of omega-3 polyunsaturated fatty acids in preventing gastrointestinal cancers: current status and future perspectives
Published in Expert Review of Anticancer Therapy, 2018
Ho-Jae Lee, Young-Min Han, Jeong Min An, Eun A. Kang, Yong Jin Park, Ji-Young Cha, Ki Baik Hahm
Lim et al. [59] showed that n-3 PUFA significantly inhibited the growth of hepatocellular carcinoma (HCC) by blocking the β-catenin and COX-2 pathways, as HCC development involves signaling via both pathways. Studies showed that DHA and EPA reduce cell viability, with cleavage of PARP, caspase-3, and caspase-9 in three HCC cell lines, namely, Hep3B, Huh-7, and HepG2 [59]. GSK-3β was also activated by dephosphorylation, which led to degradation and apoptosis of β-catenin in Hep3B cells. Furthermore, DHA inhibited PGE2 signaling via COX-2 inhibition and increased 15-hydroxyprostaglandin dehydrogenase (15-PGDH) levels. Based on the results of an in vitro study, HCC growth was confirmed in vivo by implanting murine HCC cells in Fat-1 tg mice. In wild-type mice, the tumor was formed in all mice 4 days after cell inoculation; however in the Fat-1 tg mice, small-sized tumors were observed in 50% mice, which almost disappeared 12 days after the cell inoculation [59]. Furthermore, Weylandt et al. [60] confirmed the effects of n-3 PUFA in diethylnitrosamine (DEN)-induced liver tumor model in Fat-1 tg mice. Liver tumor formation was reduced, and the expression of plasma TNF-α and liver COX-2 were significantly reduced in Fat-1 tg mice compared to in wild-type mice. In addition, lipidomic analysis revealed that the anti-inflammatory 18-hydroxyeicosapentaenoic acid (18-HEPE) and 17-hydroxydocosahexaenoic acid (17-HDHA) were present in the liver of Fat-1 tg mice. Therefore, n-3 PUFAs inhibit liver tumorigenesis, probably by reducing liver inflammation.