crocin and Kidney-Diseases

Crocin has been reported to have multiple bioactivities. However, the effect of crocin administration on caecal ligation and puncture (CLP)-induced sepsis remains unknown.. We investigated the effects of crocin on CLP-induced sepsis in mice and the underlying mechanism of action.. Compared to the CLP group, crocin treatment significantly increased the survival rate (70%, 80%, 90% vs. 30%). Crocin groups exhibited protection against liver, kidney and lung damage with mild-to-moderate morphological changes and lower indicator levels: liver (2.80 ± 0.45, 2.60 ± 0.55, 1.60 ± 0.55 vs. 5.60 ± 0.55), kidney (3.00 ± 0.71, 2.60 ± 0.55, 1.40 ± 0.55 vs. 6.20 ± 0.84) and lungs (8.00 ± 1.59, 6.80 ± 1.64, 2.80 ± 0.84 vs. 14.80 ± 1.79). The proinflammatory cytokines (IL-1β, TNF-α, IL-6 and IL-10 levels in the crocin groups) were distinctly lower and the apoptotic index showed a significant decrease. Crocin administration significantly suppressed p38 MAPK phosphorylation and inhibited NF-κB/IκBα and Bcl-2/Bax activation.. Pre-treatment with crocin confers protective effects against CLP-induced liver, kidney and lung injury, implying it to be a potential therapeutic agent.

Topics: Animals; bcl-2-Associated X Protein; Carotenoids; Disease Models, Animal; Dose-Response Relationship, Drug; Kidney Diseases; Liver Diseases; Lung Diseases; Mice; Mice, Inbred BALB C; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Proto-Oncogene Proteins c-bcl-2; Sepsis

As a powerful antioxidant compound, crocin can partially protect against renal ischemia/reperfusion (I/R) injuries. The encapsulation of components in niosomes (non-ionic surfactant-based vesicle) as nano-sized carrier systems has been proposed as they improve the solubility, stability, and bioavailability of drugs. Herein, the encapsulation of crocin in nano-niosomes and the effects of crocin-loaded nano-niosomes on renal ischemia/reperfusion-induced damages were evaluated. Nano-niosomes containing crocin were formulated by a modified heating method and were characterized for their physicochemical characteristics. Ischemia was induced by clamping the renal artery for 30 min followed by 1 or 24 h of reperfusion. Rats received an intra-arterial injection of nano-niosome-loaded crocin at the outset of reperfusion. Blood samples were taken after reperfusion to measure urea, creatinine (Cr), malondialdehyde (MDA), and superoxide dismutase (SOD) activity. The right kidney was removed for histological examination. The results showed that crocin-contain nano-niosomes have appropriate size and morphology, acceptable encapsulation efficiency, and a proper release pattern of crocin. I/R enhanced creatinine (Cr), urea, and malondialdehyde (MDA) serum levels and reduced SOD activity and histological damages in the renal tissue.

Topics: Animals; Antioxidants; Blood Urea Nitrogen; Carotenoids; Creatinine; Glutathione Peroxidase; Kidney; Kidney Diseases; Liposomes; Male; Malondialdehyde; Nanoparticles; Oxidative Stress; Protective Agents; Rats; Rats, Wistar; Renal Artery; Reperfusion Injury; Superoxide Dismutase

Doxorubicin is a drug that belongs to the anthracycline antibiotics. Nephrotoxicity is one of the serious side effects of doxorubicin treatment. Crocin, which is one of the most bioactive components of saffron, has antioxidant, anti-inflammatory, and antitumor effects. The current study was aimed at investigating the possible protective effects of crocin against doxorubicin-induced nephrotoxicity to elucidate the underlying mechanism of this effect. The study included four groups, six rats in each group: normal control, crocin control, doxorubicin, and crocin/doxorubicin. Doxorubicin and crocin/doxorubicin groups received intraperitoneal injections of doxorubicin (3.5 mg/kg twice weekly for 3 weeks). Rats in the crocin control group and the crocin/doxorubicin group were treated with intraperitoneal injections of crocin (100 mg/kg body weight per day) for 3 weeks. Biomarkers of kidney function and oxidative stress as well as the abundance of mRNA for nuclear factor-

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Biomarkers; Carotenoids; Creatinine; Cyclooxygenase 2; Doxorubicin; Kidney; Kidney Diseases; Male; NF-kappa B; Nitric Oxide Synthase Type II; Oxidative Stress; Rats, Sprague-Dawley; RNA, Messenger; Tumor Necrosis Factor-alpha

Renal Ischemia (RI) usually develops as a secondary manifestation of hypertension, various cardiovascular disorders and renal transplantation. It exerts hypoxic oxidative stress to kidneys, together with stimulation of several immune-mediated inflammatory cascades. Such events eventually damage renal tubules and glomeruli, driving acute kidney injury (AKI) and ultimately, renal failure. Crocin; the main bioactive constituent of Crocus sativus extract has been reported to demonstrate numerous pharmacological merits. In the current study, unilateral renal ischemia reperfusion injury (URIRI) was induced in rats by unilateral clamping of the left renal pedicle for 45 min followed by 24 h of reperfusion. Daily pre-treatment with crocin (20 mg/kg, orally) for 7 days, significantly improved all signs of renal injury. Biochemically, kidney functions; including serum creatinine (Sr Cr), blood urea nitrogen (BUN), proteinuria and creatinine clearance (Cr Cl) significantly improved. Inflammatory biomarkers; serum lactate dehydrogenase (LDH) and kidney nitric oxide (Nos) contents significantly declined. Oxidant/antioxidant balance was significantly restored; manifested in recovery of renal superoxide dismutase (SOD) activity, glutathione (GSH) concentration, malondialdehyde (MDA) content and restoration of serum catalase activity. Kidney contents of inflammatory cytokine interleukin-6 (IL6) and toll-like receptors 4 (TLR4) significantly declined as well. Histopathologically, crocin pretreatment resulted in signs of improvement with minimal renal lesions with significant decrease in renal inflammatory cells count. In conclusion, crocin induced restoration of normal kidney functions is mediated through multiple mechanisms including mainly attenuation of oxidative stress and inflammation via down-regulation of renal TLR4 and IL6 expression.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Blood Urea Nitrogen; Carotenoids; Catalase; Glutathione; Interleukin-6; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Male; Malondialdehyde; Nitric Oxide; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase; Toll-Like Receptor 4

Nephropathy is a serious complication of metabolic syndrome (MS), a global epidemic disorder. This study was undertaken to investigate the actions of diosmin and crocin, two natural ingredients, on diabetic nephropathy in a rat model of MS and the underlying mechanism(s). Metabolic syndrome was induced by the addition of 10% fructose to drinking water and placing the rats on high-salt diet for 16 weeks. Diosmin and Crocin were orally administrated daily for 10 weeks starting at week 6. At the end of study, arterial blood pressure was non-invasively recorded. Urine, serum and kidneys were collected for renal function, oxidative stress, glycemic parameters, inflammatory markers and histological analysis. Both Diosmin and Crocin improved insulin resistance, decreased blood pressure, uric acid, lipoproteins and blocked diabetic nephropathy as indicated by reduction of albumin excretion rate and albumin/creatinine ratio. They alleviated the impaired filtration in MS as indicated by increased creatinine clearance. They also ameliorated oxidative stress and the low-grade 1inflammation as indicated by reduction of serum TNF-α and inflammatory cells. These observations suggest that both Diosmin and Crocin alleviate metabolic syndrome and the associated nephropathy in rats, possibly, through inhibiting oxidative stress and inflammation.

Topics: Animals; Blood Glucose; Blood Pressure; Carotenoids; Diosmin; Drug Therapy, Combination; Glycation End Products, Advanced; Inflammation; Insulin; Insulin Resistance; Kidney Diseases; Kidney Glomerulus; Lipids; Male; Malondialdehyde; Metabolic Syndrome; Oxidative Stress; Rats, Wistar; Tumor Necrosis Factor-alpha; Uric Acid

The present study was conducted to investigate the changes in rat kidney tissues after administration of tartrazine (T) and crocine (Cr). The latter was applied for its protective properties. The present study was conducted with the approval of Inonu University, Faculty of Medicine, Experimental Animals Ethics Committee. Forty rats were randomly divided into 4 equal groups (Control, T, Cr, T + Cr). At the end of the experiment, the rats were decapitated. Biochemical and histopathological studies were conducted on excised rat kidney tissues. It was determined that there was a significant increase in MDA, TOS, SOD, CAT, Bun, Creatinine levels in tartrazine administered rat kidney tissues for 21 days, while GSH and TAS levels decreased (P ≤ 0.05) when compared to all other groups. On the other hand, it was identified that Cr administration statistically significantly increased GSH and TAS levels in rat kidney tissues when compared to all other groups and decreased MDA and TOS levels to control group levels (P < 0.05). T group kidney sections exhibited different degrees of collapse in the glomeruli. In most sections, different levels of inflammatory cell infiltration and vascular and capillary congestion were detected in peritubular interstitial tissue. It was determined that T leads to adverse effects on rat kidney tissues. Administration of Cr + T prevented T induced nephrotoxicity. Thus, it was concluded that Cr could be utilized as a new type of anti-tartrazine toxicity agent.

Topics: Animals; Antioxidants; Blood Urea Nitrogen; Carotenoids; Catalase; Creatinine; Female; Glutathione; Kidney; Kidney Diseases; Malondialdehyde; Oxidative Stress; Protective Agents; Rats; Rats, Wistar; Superoxide Dismutase; Tartrazine

We used an experimental model in the rat to examine the effects of long-term treatment with crocin, a glycosylated carotenoid from the stigmas of the saffron crocus, on colon cancer. BD-IX rats were divided into four groups: Groups G1 and G2, designated "cancer groups," were used to study the effects of crocin on the progression of colon cancer, and Groups G3 and G4, designated "toxicity groups," were used to study the effects of the treatment on metabolic processes and the parenchyma. DHD/K12-PROb cells were injected subcutaneously into the chest of Group G1 and G2 animals. From 1 to 13 weeks after inoculation, animals in Groups G2 and G4 received a weekly injection of crocin (400 mg/kg body wt s.c.). Animals in Groups G1 and G3 received no treatment. In addition, lines of animal and human colon adenocarcinoma cells (DHD/K12-PROb and HT-29) were used to perform assays in vitro to examine the cytotoxicity of crocin. Life span was extended and tumor growth was slower in crocin-treated female rats, but no significant antitumor effect was found in male rats. Acute tubular necrosis was found in all kidney samples from crocin-treated animals, but slight signs of nephrotoxicity were found by biochemical analysis of the serum. In assays in vitro, crocin had a potent cytotoxic effect on human and animal adenocarcinoma cells (HT-29 and DHD/K12-PROb cells, 50% lethal dose = 0.4 and 1.0 mM, respectively). Treated cells exhibited a remarkable loss of cytoplasm and wide cytoplasmic vacuole-like areas. In conclusion, long-term treatment with crocin enhances survival selectively in female rats with colon cancer without major toxic effects. The effects of crocin might be related to its strong cytotoxic effect on cultured tumor cells.

Topics: Adenocarcinoma; Animals; Carotenoids; Cell Survival; Colonic Neoplasms; Female; Humans; Kidney Diseases; Kidney Tubules; Liliaceae; Male; Necrosis; Neoplasm Transplantation; Rats; Tumor Cells, Cultured