sodium-bicarbonate and Inflammation

Metabolic acidosis is a frequent complication of chronic kidney disease. Although it is known to appear at advanced stages, many studies suggest a state of "global protonic retention" starting at early stages of the disease, responsible of tissue damage, particularly musculoskeletal, alteration of protidic metabolism and endocrine disorders, promoting malnutrition and chronic inflammation, and finally increasing mortality. The majority of international recommandations suggest of supplementation by alkali, most of the time by sodium bicarbonate, to struggle against this complication. An interesting alternative to correct acidosis would consist on the modulation of the endogenous production of acid by playing with the alimentary incomes. In fact, it has been demonstrated that some different types of food produce or consume protons during their metabolism. Low protein diet and rich fresh fruits and vegetables diet would manage to correct at least as well as the supplementation by sodium bicarbonate the metabolic acidosis, and to struggle against its complications, noteworthy by slowing the decline of glomerular filtration rate by limiting the toxic adaptative fibrotic mechanisms, demonstrated by the decrease of urinary tubulo-interstitial suffering markers. Of the condition of being well led, those diets do not seem to expose patients to an over-risk of malnutrition or hyperkaliemia. They therefore appear to be an attractive alternative, efficiency and safe, to fight against chronic kidney disease metabolic acidosis and its complications.

Topics: Acidosis; Chronic Kidney Disease-Mineral and Bone Disorder; Combined Modality Therapy; Diet, Protein-Restricted; Dietary Proteins; Fruit; Humans; Hyperkalemia; Hypoalbuminemia; Inflammation; Malnutrition; Nutrition Policy; Protons; Renal Insufficiency, Chronic; Sarcopenia; Sodium Bicarbonate; Vegetables

To assess the anti-plaque effect of a high concentration sodium bicarbonate dentifrice on plaque formation, and gingivitis, as compared to a control toothpaste, irrespective of individual brushing technique and plaque quality.. The experimental gingivitis model, with a split-mouth design was used to assess the anti-plaque effect of a high concentration sodium bicarbonate dentifrice on plaque formation. By producing individual fitted trays, the toothpaste was applied in the test quadrant and a control dentifrice in the contralateral. The participants used the individual fitted trays for 1 min every morning and evening, for 21 days. In this period, the participants was only allowed to brush the teeth in the opposite jaw, as usual. Twenty healthy individuals successfully completed the study.. At 21 days, there was no statistically significant difference between test quadrant and control quadrant with regard to plaque indices, gingival index and number of bleeding sites.. This study demonstrated that the high concentration sodium bicarbonate dentifrice used did not produce statistically significant anti-plaque effect compared to the control dentifrice, in terms of Plaque- and Gingival Indices, number of bleeding sites or by Quigely and Hein, the Turesky modification Plaque Index, irrespective of brushing technique and individual plaque quality.. Regional Committee for Medical Research and Ethics, South-East Norway in 2021 (REK.2021/370116).. NCT05441371 (First registered 09/06/2022, First posted 01/07/2022) ( http://www.. gov ). (Retrospectively registered).

Topics: Bicarbonates; Dental Plaque; Dental Plaque Index; Dentifrices; Double-Blind Method; Gingivitis; Humans; Inflammation; Sodium Bicarbonate; Toothpastes

Macrophages, which develop by changing their functions according to various environmental conditions and stimuli, defend against the pathogens and play roles in homoeostasis and disease states. Bicarbonate (HCO3-) is important in the maintenance of intracellular and extracellular pH in the body. However, the effects of bicarbonate on macrophage function have not been examined. In this study, we investigated the effects of bicarbonate on macrophage activation in lipopolysaccharide (LPS) and interferon (IFN)-γ (LPS + IFN-γ)-stimulated murine macrophage-like RAW264.7 cells. The expression of the interleukin (IL)-6, inducible nitric oxide (NO) synthase and cyclooxygenase-2 genes was enhanced by sodium bicarbonate (NaHCO3) in a concentration-dependent manner in LPS + IFN-γ-stimulated RAW264.7 cells. The production of IL-6, NO2- and prostaglandin E2 was also increased by treatment with NaHCO3 in these cells. Moreover, NaHCO3-mediated elevation of inflammatory gene expression was abrogated by solute carrier (SLC) transporter inhibitors. Furthermore, its NaHCO3-mediated activation was negated by a JAK inhibitor , tofacitinib. NaHCO3-enhanced phosphorylation of STAT1, and its enhancement was abrogated by pre-treating with SLC transporter inhibitors in LPS + IFN-γ-stimulated RAW264.7 cells. In addition, similar results were obtained in murine bone marrow-derived macrophages. These results indicate that bicarbonate enhanced the inflammatory response through the JAK/STAT signalling in LPS + IFN-γ-stimulated macrophages.

Topics: Animals; Cyclooxygenase 2; Gene Expression; Inflammation; Interferon-gamma; Interleukin-6; Janus Kinase Inhibitors; Janus Kinases; Lipopolysaccharides; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred C57BL; Nitric Oxide; Piperidines; Pyrimidines; RAW 264.7 Cells; Recombinant Proteins; Signal Transduction; Sodium Bicarbonate; STAT1 Transcription Factor

Administration of ammonium chloride aggravates, while short-term administration of sodium or potassium bicarbonate lessens the development of polycystic kidney disease in Han:SPRD rats. We have conducted studies to determine whether the protection afforded by the administration of sodium bicarbonate is sustained and prevents development of uremia during chronic administration and whether the effects of the administration of ammonium chloride and sodium bicarbonate are also observed in a different model of polycystic kidney disease, the CD1-pcy/pcy mouse. We found that chronic administration of 200 mM sodium bicarbonate to Han:SPRD rats inhibited cystic enlargement and prevented the subsequent development of interstitial inflammation, chronic fibrosis, and uremia. We also found that, while the administration of ammonium chloride has similar effects in Han:SPRD rats and CD1-pcy/pcy mice, the administration of sodium bicarbonate is only protective in the Han:SPRD rats. This probably reflects differences in these models (predominately involvement of proximal tubules in Han:SPRD rats and of collecting ducts and distal tubules in pcy/pcy mice) and the different location and nature of the renal metabolic responses to the administration of acid or alkaline load.

Topics: Ammonia; Ammonium Chloride; Animals; Bicarbonates; Disease Models, Animal; Female; Fibrosis; Inflammation; Kidney; Male; Mice; Mice, Inbred Strains; Microscopy, Electron, Scanning; Organ Size; Polycystic Kidney Diseases; Rats; Rats, Inbred Strains; Sodium Bicarbonate; Species Specificity; Time Factors; Uremia

Approximately 30% of patients affected of PCT present scleroderma-like lesion of the skin. Two cases of PCT, presenting scleroderma-like lesions are reported. The patients were diabetic but not alcoholic and tolerate relatively well sunshine. Porphyrin elimination diminished with urine alkalinization and phlebotomies, and the scleroderma-like lesions improved with N-acetyl-hydroxy-proline administration.

Topics: Aged; Animals; Bicarbonates; Cricetinae; Diabetes Complications; Diagnosis, Differential; Hemorrhage; Humans; Hydroxyproline; Inflammation; Male; Middle Aged; Porphyrias; Scleroderma, Systemic; Skin; Skin Diseases; Sodium; Sodium Bicarbonate