astaxanthine and Kidney-Diseases

The blockade of the progression or onset of pathological events is essential for the homeostasis of an organism. Some common pathological mechanisms involving a wide range of diseases are the uncontrolled inflammatory reactions that promote fibrosis, oxidative reactions, and other alterations. Natural plant compounds (NPCs) are bioactive elements obtained from natural sources that can regulate physiological processes. Inflammation is recognized as an important factor in the development and evolution of chronic renal damage. Consequently, any compound able to modulate inflammation or inflammation-related processes can be thought of as a renal protective agent and/or a potential treatment tool for controlling renal damage. The objective of this research was to review the beneficial effects of bioactive natural compounds on kidney damage to reveal their efficacy as demonstrated in clinical studies.. This systematic review is based on relevant studies focused on the impact of NPCs with therapeutic potential for kidney disease treatment in humans.. Clinical studies have evaluated NPCs as a different way to treat or prevent renal damage and appear to show some benefits in improving OS, inflammation, and antioxidant capacity, therefore making them promising therapeutic tools to reduce or prevent the onset and progression of KD pathogenesis.. This review shows the promising clinical properties of NPC in KD therapy. However, more robust clinical trials are needed to establish their safety and therapeutic effects in the area of renal damage.

Topics: Antioxidants; Berberine; Beta vulgaris; Betalains; Biological Products; Catechin; Curcumin; Disulfides; Flavonoids; Humans; Isothiocyanates; Kidney; Kidney Diseases; Plant Extracts; Pomegranate; Protective Agents; Resveratrol; Sulfinic Acids; Sulfoxides; Xanthophylls

Loss of peritubular capillaries is a notable feature of progressive renal interstitial fibrosis. Astaxanthin (ASX) is a natural carotenoid with various biological activities. The present study aimed to evaluate the effect of ASX on unilateral ureteral obstruction (UUO)‑induced renal fibrosis in mice. For that purpose, mice were randomly divided into five treatment groups: Sham, ASX 100 mg/kg, UUO, UUO + ASX 50 mg/kg and UUO + ASX 100 mg/kg. ASX was administered to the mice for 7 or 14 days following UUO. The results demonstrated that UUO‑induced histopathological changes in the kidney tissue were prevented by ASX. Renal function was improved by ASX treatment, as evidenced by decreased blood urea nitrogen and serum creatinine levels. Furthermore, the extent of renal fibrosis and collagen deposition induced by UUO was suppressed by ASX. The levels of collagen I, fibronectin and α‑smooth muscle actin were increased by UUO in mice or by transforming growth factor (TGF)‑β1 treatment in NRK‑52E cells, and were reduced by ASX administration. In addition, ASX inhibited the UUO‑induced decrease in peritubular capillary density by upregulating vascular endothelial growth factor and downregulating thrombospondin 1 levels. Inactivation of the TGF‑β1/Smad signaling pathway was involved in the anti‑fibrotic mechanism of ASX in UUO mice and TGF‑β1‑treated NRK‑52E cells. In conclusion, ASX attenuated renal interstitial fibrosis and peritubular capillary rarefaction via inactivation of the TGF‑β1/Smad signaling pathway.

Topics: Animals; Biomarkers; Biopsy; Cell Line; Disease Models, Animal; Fibrinolytic Agents; Fibrosis; Kidney Diseases; Male; Mice; Microvascular Rarefaction; Rats; Signal Transduction; Smad Proteins; Transforming Growth Factor beta1; Ureteral Obstruction; Vascular Endothelial Growth Factor A; Xanthophylls

Renal fibrosis is a common pathological hallmark of chronic kidney disease, and no effective treatment is clinically available to manage its progression. Astaxanthin was recently found to be anti-fibrotic, but its effect on renal fibrosis remains unclear.. C57BL/6J mice were subjected to unilateral ureteral obstruction and intragastrically administered astaxanthin. Histopathology and immunohistochemistry were performed to evaluate renal fibrosis. Flow cytometry was used to examine lymphocyte accumulation in the fibrotic kidneys. Western blotting, real-time qPCR, and immunofluorescence were performed to cover the underlying mechanism concerning astaxanthin treatment during renal fibrosis.. Oral administration of astaxanthin effectively alleviates renal fibrosis in mice. In vitro, astaxanthin inhibited fibroblast activation by modulating Smad2, Akt and STAT3 pathways and suppressed epithelial-to-mesenchymal transition in renal tubular epithelial cells through Smad2, snail, and β-catenin. Moreover, astaxanthin significantly induced the rapid accumulation of CD8. These findings highlight the beneficial effect of astaxanthin on fibroblast activation, epithelial-to-mesenchymal transition, and CD8. These data indicate that astaxanthin could serve as a therapeutic strategy to treat renal fibrotic conditions.

Topics: Animals; beta Catenin; CD8-Positive T-Lymphocytes; Epithelial-Mesenchymal Transition; Fibrosis; Interferon-gamma; Kidney Diseases; Male; Mice; Mice, Inbred C57BL; Myofibroblasts; Proto-Oncogene Proteins c-akt; Smad2 Protein; Snail Family Transcription Factors; STAT3 Transcription Factor; Xanthophylls

We evaluated the effect of astaxanthin (ASX) and vitamin E (vit E) on colistin methanesulfonate (CMS) induced-nephrotoxicity in rats.. Animals were treated with sterile saline, 300000 or 450 000 IU/kg/day of CMS, CMS + ASX (20 mg/kg), CMS + vit E (100 mg/kg), or CMS + 1 ml/kg olive oil (OO) for 7 days. The plasma/urine creatinine (Cr) level, urine γ-glutamyl-transferase (GGT) level, and renal tissue activities in malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reductase (GSH), as well as renal histology were performed.. CMS induced a tubular damage, increased the GGT and MDA levels, and decreased the activities of SOD, CAT, GPx and GSH. Co-treatment with ASX or vit E restored all biochemical parameters cited above and improved the histopathological damage.. Nephrotoxicity induced by CMS might be due to oxidative damage. The improvement by ASX or vit E seems to be related to their antioxidant properties.

Topics: Animals; Anti-Bacterial Agents; Antioxidants; Catalase; Colistin; Creatinine; gamma-Glutamyltransferase; Glutathione Peroxidase; Glutathione Reductase; Kidney; Kidney Diseases; Male; Malondialdehyde; Rats, Wistar; Superoxide Dismutase; Vitamin E; Xanthophylls

To study the effects of astaxanthin on renal fibrosis and apoptosis induced by partial unilateral ureteral obstruction (UUO) in rats.. Ninety-six male adult SD rats were randomized into 6 equal groups, namely the blank control group, sham-operated group, UUO group, and astaxanthin group at high, medium, and low doses. Left ureteral ligation was performed in UUO and astaxanthin groups, and two days before the operation, the rats in astaxanthin groups were lavaged with 25, 50, or 100 mg/kg astaxanthin daily for 14 days, while the same volume of saline was given to rats in UUO group and sham-operated group. Renal pathological in the rats was observed with HE staining, and the expression levels of TGF-β1, SGK1, and CTGF in the left kidney were detected immunohistochemically; the expression level of Bcl-2 and Bax were detected using Bcl-2 and Bax detection kits.. Compared to UUO group, high- and medium-dose astaxanthin groups showed obviously ameliorated renal pathologies and reduced expressions of TGF-β1, SGK1, and CTGF in the left kidney with lessened renal cell apoptosis.. Astaxanthin can reduce UUO-induced renal fibrosis and renal cell apoptosis, demonstrating the renoprotective effect of astaxanthin against renal fibrosis.

Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Connective Tissue Growth Factor; Fibrosis; Immediate-Early Proteins; Kidney; Kidney Diseases; Male; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta1; Ureteral Obstruction; Xanthophylls

Astaxanthin is a carotenoid with powerful antioxidant properties that exists naturally in various plants, algae, and seafood. The purpose of the present study is to examine the protective action of astaxanthin against high-glucose-induced oxidative stress, inflammation, and apoptosis in proximal tubular epithelial cells (PTECs). To assess the efficacy of astaxanthin, several key markers and activities were measured, including lipid peroxidation, total reactive species (RS), superoxide (*O(2)), nitric oxide (NO*), and peroxynitrite (ONOO(-)), as well as expressions of inflammatory proteins, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-kappaB) nuclear translocation, and levels of Bcl2/Bax protein. Results showed that astaxanthin effectively suppressed lipid peroxidation, total RS, *O(2), NO*, ONOO(-), iNOS and COX-2 protein levels, NF-kappaB nuclear translocation, and pro-apototic Bax, whereas it increased anti-apoptotic Bcl2 protein levels. On the basis of these findings, it was concluded that in PTECs, astaxanthin has a protective efficacy against several deleterious effects caused by high glucose exposure and proposed that astaxanthin should be explored further as a potential antidiabetic remedy for the treatment of diabetic nephropathy.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Apoptosis; Biomarkers; Cell Line; Epithelial Cells; Free Radical Scavengers; Glucose; Inflammation; Kidney Diseases; Kidney Tubules, Proximal; Oxidative Stress; Swine; Xanthophylls

Reactive oxygen species are implicated as mediators of tissue damage in the acute renal failure induced by inorganic mercury. Astaxanthin (ASX), a carotenoid with potent antioxidant properties, exists naturally in various plants, algae, and seafoods. This paper evaluated the ability of ASX to prevent HgCl(2) nephrotoxicity. Rats were injected with HgCl(2) (0 or 5 mg/kg b.w., sc) 6h after ASX had been administered (0, 10, 25, or 50mg/kg, by gavage) and were killed 12h after HgCl(2) exposure. Although ASX prevented the increase of lipid and protein oxidation and attenuated histopathological changes caused by HgCl(2) in kidney, it did not prevent creatinine increase in plasma and delta-aminolevulinic acid dehydratase inhibition induced by HgCl(2). Glutathione peroxidase and catalase activities were enhanced, while superoxide dismutase activity was depressed in HgCl(2)-treated rats when compared to control and these effects were prevented by ASX. Our results indicate that ASX could have a beneficial role against HgCl(2) toxicity by preventing lipid and protein oxidation, changes in the activity of antioxidant enzymes and histopathological changes.

Topics: Animals; Antioxidants; Biomarkers; Glutathione Transferase; Kidney; Kidney Diseases; Kidney Function Tests; Lipid Peroxidation; Male; Mercuric Chloride; Necrosis; Oxidative Stress; Porphobilinogen Synthase; Protein Carbonylation; Rats; Rats, Wistar; Sulfhydryl Compounds; Thiobarbituric Acid Reactive Substances; Xanthophylls