Pharmacological properties of Hoya (Apocynaceae): a systematic review.

In tropical forests, Hoya, a plant with significant indigenous medicinal applications, has been underexplored in pharmacological studies. This systematic review meticulously investigates the diverse pharmacological effects exhibited by various Hoya species on human health. A comprehensive literature search, encompassing Scopus, ScienceDirect, and SpringerLink databases, employed specific keyword combinations ('Hoya' and 'pharmacological properties' OR 'pharmacology property'). The included studies exclusively focused on Hoya's impact on human health. The findings underscore Hoya's potential as a medicinal plant, demonstrating promising attributes such as anticancer, antibacterial, antioxidant, anti-inflammatory, anti-diabetic, antinociceptive, and parasympatholytic effects. Despite these promising indications, the review underscores the necessity for further in vivo investigations to fully unlock Hoya's therapeutic potential. A comprehensive understanding of its mechanisms of action, efficacy, and safety in living systems is imperative for realising its holistic therapeutic benefits.

Probability of Concurrent Deficiency of Vitamin D and Iron in Hypothyroidism: A Cross-Sectional Study.

BACKGROUND: Hypothyroidism is the most common pathophysiological condition that affects mostly females in both developed and developing countries. Data on hypothyroidism among adult females are essential to understand the underactive status of the thyroid gland among the female population and its correlated effects on a deficiency of vitamin D and iron, as effective prevention of osteoporotic changes and iron deficiency anemia is possible. Therefore, the present study was designed to investigate the probability of concurrent iron and vitamin D deficiency among the adult hypothyroid female population of Abu Dhabi, UAE. MATERIALS AND METHODS: This cross-sectional study was carried out from September 2019 to July 2021 among 500 adult females aged 18 to 45 years old in Sheikh Shakhbout Medical City (SSMC) and Sheikh Khalifa Medical City (SKMC), Abu Dhabi, UAE. After obtaining written informed consent, subjects' demographic characteristics (sun exposure, dressing code, food consumption), anthropometry (height, weight, BMI), and biochemical parameters (thyroid profile, vitamin D profile, iron profile, and blood indices) were measured. RESULTS: In this study, serum vitamin D and iron levels were significantly (p<0.01) decreased in the hypothyroid female group (study group). The serum vitamin D and iron levels showed a significant negative (p<0.01) correlation with thyroid-stimulating hormone (TSH). Out of 250 study group participants, 61 had a concurrent deficiency of serum vitamin D and iron, yielding a probability (P of low vitamin D and iron and hypothyroidism) of 0.244, which indicates that if 1000 hypothyroid patients are tested for serum vitamin D and iron levels, 24 patients are probable to have low vitamin D and iron. CONCLUSION: The study concluded that vitamin D and iron bi-deficiency were observed in adult hypothyroid females in Abu Dhabi, UAE. So, the routine check-up of thyroid function and vitamin D and iron profiles should be done early. Therefore, early vitamin D and iron deficiencies can be detected, and supplements can be given to prevent further health complications like osteoporosis and iron deficiency anemia.

Short-chain fatty acids augment rat duodenal mucosal barrier function.

NEW FINDINGS: What is the central question of this study? Small intestinal epithelium is exposed to high concentrations of short-chain fatty acids (SCFAs), but their role in regulating intestinal mucosal barrier function and motility is not fully understood. What is the main finding and its importance? By perfusing the duodenal segment in anaesthetized rats, we show that acetate and propionate significantly decrease mucosal paracellular permeability and transepithelial net fluid flux and increase mucosal bicarbonate secretion. Likewise, SCFAs administered i.v. decrease mucosal permeability but decrease bicarbonate secretion. Altered luminal chemosensing or aberrant signalling in response to SCFAs might contribute to symptoms observed in patients with suppressed mucosal barrier function. Short-chain fatty acids (SCFAs) are produced by bacterial fermentation in the large intestine, particularly from diets containing fibres and carbohydrates. The small intestinal epithelium is exposed to SCFAs derived mainly from oral bacteria or food supplementation. Although luminal nutrients are important in regulation of intestinal functions, the role of SCFAs in regulation of small intestinal mucosal barrier function and motility has not been fully described. The aim of the present study was to elucidate the effects of acetate and propionate on duodenal mucosal barrier function and motility. Rats were anaesthetized with thiobarbiturate, and a 30 mm segment of proximal duodenum with an intact blood supply was perfused. The effects on duodenal bicarbonate secretion, blood-to-lumen clearance of 51 Cr-EDTA, motility and transepithelial net fluid flux were investigated. Perfusion of the duodenum with acetate or propionate significantly decreased mucosal paracellular permeability and transepithelial net fluid flux and significantly increased bicarbonate secretion. Acetate or propionate administered as an i.v. infusion decreased the mucosal paracellular permeability, but significantly decreased bicarbonate secretion. Luminal SCFAs changed the duodenal motility pattern from migrating motor complexes to fed patterns. Systemic administration of glucagon-like peptide-2 induced increases in both bicarbonate secretion and net fluid absorption, but did not change motility. Glucagon-like peptide-2 infusion during luminal perfusion of SCFAs significantly reduced the motility. In conclusion, SCFAs decreased duodenal paracellular permeability and net fluid flux. Short-chain fatty acids induced opposite effects on bicarbonate secretion after luminal and i.v. administration. Presence of SCFAs in the lumen induces fed motility patterns. Altered luminal chemosensing and aberrant signalling in response to SCFAs might contribute to symptoms observed in patients with suppressed barrier function.

Neuropeptide S reduces duodenal bicarbonate secretion and ethanol-induced increases in duodenal motility in rats.

Alcohol disrupts the intestinal mucosal barrier by inducing metabolic and functional changes in epithelial cells. Recently, we showed that neuropeptide S (NPS) decreases duodenal motility and increases mucosal paracellular permeability, suggesting a role of NPS in the pathogenesis of disorders and dysfunctions in the small intestine. The aim of the present study was to investigate the effects of NPS on ethanol- and HCl-induced changes of duodenal mucosal barrier function and motility. Rats were anaesthetized with thiobarbiturate, and a 30-mm segment of the proximal duodenum with an intact blood supply was perfused in situ. The effects on duodenal bicarbonate secretion, the blood-to-lumen clearance of 51Cr-EDTA, motility and transepithelial net fluid flux were investigated. Intravenous (i.v.) administration of NPS significantly reduced duodenal mucosal bicarbonate secretion and stimulated mucosal transepithelial fluid absorption, mechanisms dependent on nitrergic signaling. NPS dose-dependently reduced ethanol-induced increases in duodenal motility. NPS (83 pmol·kg-1·min-1, i.v.) reduced the bicarbonate and fluid secretory response to luminal ethanol, whereas a 10-fold higher dose stimulated fluid secretion but did not influence bicarbonate secretion. In NPS-treated animals, duodenal perfusion of acid (pH 3) induced greater bicarbonate secretory rates than in controls. Pre-treating animals with Nω-nitro-L-arginine methyl ester (L-NAME) inhibited the effect of NPS on bicarbonate secretion. In response to luminal acid, NPS-treated animals had significantly higher paracellular permeability compared to controls, an effect that was abolished by L-NAME. Our findings demonstrate that NPS reduces basal and ethanol-induced increases in duodenal motility. In addition, NPS increases luminal alkalinization and mucosal permeability in response to luminal acid via mechanisms that are dependent on nitric oxide signaling. The data support a role for NPS in neurohumoral regulation of duodenal mucosal barrier function and motility.

Neuropeptide S inhibits gastrointestinal motility and increases mucosal permeability through nitric oxide.

Neuropeptide S (NPS) receptor (NPSR1) polymorphisms are associated with enteral dysmotility and inflammatory bowel disease (IBD). This study investigated the role of NPS in conjunction with nitrergic mechanisms in the regulation of intestinal motility and mucosal permeability. In rats, small intestinal myoelectric activity and luminal pressure changes in small intestine and colon, along with duodenal permeability, were studied. In human intestine, NPS and NPSR1 were localized by immunostaining. Pre- and postprandial plasma NPS was measured by ELISA in healthy and active IBD humans. Effects and mechanisms of NPS were studied in human intestinal muscle strips. In rats, NPS 100-4,000 pmol·kg(-1)·min(-1) had effects on the small intestine and colon. Low doses of NPS increased myoelectric spiking (P < 0.05). Higher doses reduced spiking and prolonged the cycle length of the migrating myoelectric complex, reduced intraluminal pressures (P < 0.05-0.01), and increased permeability (P < 0.01) through NO-dependent mechanisms. In human intestine, NPS localized at myenteric nerve cell bodies and fibers. NPSR1 was confined to nerve cell bodies. Circulating NPS in humans was tenfold below the ∼0.3 nmol/l dissociation constant (Kd) of NPSR1, with no difference between healthy and IBD subjects. In human intestinal muscle strips precontracted by bethanechol, NPS 1-1,000 nmol/l induced NO-dependent muscle relaxation (P < 0.05) that was sensitive also to tetrodotoxin (P < 0.01). In conclusion, NPS inhibits motility and increases permeability in neurocrine fashion acting through NO in the myenteric plexus in rats and humans. Aberrant signaling and upregulation of NPSR1 could potentially exacerbate dysmotility and hyperpermeability by local mechanisms in gastrointestinal functional and inflammatory reactions.

The ethanol-induced stimulation of rat duodenal mucosal bicarbonate secretion in vivo is critically dependent on luminal Cl-.

Alcohol may induce metabolic and functional changes in gastrointestinal epithelial cells, contributing to impaired mucosal barrier function. Duodenal mucosal bicarbonate secretion (DBS) is a primary epithelial defense against gastric acid and also has an important function in maintaining the homeostasis of the juxtamucosal microenvironment. The aim in this study was to investigate the effects of the luminal perfusion of moderate concentrations of ethanol in vivo on epithelial DBS, fluid secretion and paracellular permeability. Under thiobarbiturate anesthesia, a ∼30-mm segment of the proximal duodenum with an intact blood supply was perfused in situ in rats. The effects on DBS, duodenal transepithelial net fluid flux and the blood-to-lumen clearance of 51Cr-EDTA were investigated. Perfusing the duodenum with isotonic solutions of 10% or 15% ethanol-by-volume for 30 min increased DBS in a concentration-dependent manner, while the net fluid flux did not change. Pre-treatment with the CFTR inhibitor CFTRinh172 (i.p. or i.v.) did not change the secretory response to ethanol, while removing Cl- from the luminal perfusate abolished the ethanol-induced increase in DBS. The administration of hexamethonium (i.v.) but not capsazepine significantly reduced the basal net fluid flux and the ethanol-induced increase in DBS. Perfusing the duodenum with a combination of 1.0 mM HCl and 15% ethanol induced significantly greater increases in DBS than 15% ethanol or 1.0 mM HCl alone but did not influence fluid flux. Our data demonstrate that ethanol induces increases in DBS through a mechanism that is critically dependent on luminal Cl- and partly dependent on enteric neural pathways involving nicotinic receptors. Ethanol and HCl appears to stimulate DBS via the activation of different bicarbonate transporting mechanisms.