1.Curcumin Inhibits the Activation of Immunoglobulin E-Mediated Mast Cells and Passive Systemic Anaphylaxis in Mice by Reducing Serum Eicosanoid and Histamine Levels.
Xian LI ; Yue LU ; Ye JIN ; Jong Keun SON ; Seung Ho LEE ; Hyeun Wook CHANG
Biomolecules & Therapeutics 2014;22(1):27-34
Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cgamma1 (PLCgamma1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-kappaB (NF-kappaB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.
Administration, Oral
;
Anaphylaxis*
;
Animals
;
Arachidonate 5-Lipoxygenase
;
Curcuma
;
Curcumin*
;
Cyclooxygenase 2
;
Histamine*
;
Immunoglobulin E
;
Immunoglobulins*
;
Leukotriene C4
;
Mast Cells*
;
Mice*
;
Mitogen-Activated Protein Kinases
;
Phospholipases
;
Phosphorylation
;
Prostaglandin D2
2.Curcumin Inhibits the Activation of Immunoglobulin E-Mediated Mast Cells and Passive Systemic Anaphylaxis in Mice by Reducing Serum Eicosanoid and Histamine Levels.
Xian LI ; Yue LU ; Ye JIN ; Jong Keun SON ; Seung Ho LEE ; Hyeun Wook CHANG
Biomolecules & Therapeutics 2014;22(1):27-34
Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cgamma1 (PLCgamma1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-kappaB (NF-kappaB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.
Administration, Oral
;
Anaphylaxis*
;
Animals
;
Arachidonate 5-Lipoxygenase
;
Curcuma
;
Curcumin*
;
Cyclooxygenase 2
;
Histamine*
;
Immunoglobulin E
;
Immunoglobulins*
;
Leukotriene C4
;
Mast Cells*
;
Mice*
;
Mitogen-Activated Protein Kinases
;
Phospholipases
;
Phosphorylation
;
Prostaglandin D2
3.Post-treatment Effects of Erythropoietin and Nordihydroguaiaretic Acid on Recovery from Cisplatin-induced Acute Renal Failure in the Rat.
Dong Won LEE ; Ihm Soo KWAK ; Soo Bong LEE ; Sang Heon SONG ; Eun Young SEONG ; Byeong Yun YANG ; Min Young LEE ; Mee Young SOL
Journal of Korean Medical Science 2009;24(Suppl 1):S170-S175
5-Lipoxygenase inhibitor and human recombinant erythropoietin might accelerate renal recovery in cisplatin-induced acute renal failure rats. Male Sprague-Dawley rats were randomized into four groups: 1) normal controls; 2) Cisplatin group-cisplatin induced acute renal failure (ARF) plus vehicle treatment; 3) Cisplatin+nordihydroguaiaretic acid (NDGA) group-cisplatin induced ARF plus 5-lipoxygenase inhibitor treatment; 4) Cisplatin+erythropoietin (EPO) group-cisplatin induced ARF plus erythropoietin treatment. On day 10 (after 7 daily injections of NDGA or EPO), urea nitrogen and serum Cr concentrations were significantly lower in the Cisplatin+NDGA and Cisplatin+EPO groups than in the Cisplatin group, and 24 hr urine Cr clearances were significantly higher in the Cisplatin+EPO group than in the Cisplatin group. Semiquantitative assessments of histological lesions did not produce any significant differences between the three treatment groups. Numbers of PCNA(+) cells were significantly higher in Cisplatin, Cisplatin+NDGA, and Cisplatin+EPO groups than in normal controls. Those PCNA(+) cells were significantly increased in Cisplatin+NDGA group. These results suggest that EPO and also NDGA accelerate renal function recovery by stimulating tubular epithelial cell regeneration.
Animals
;
Arachidonate 5-Lipoxygenase/administration & dosage
;
Blood Urea Nitrogen
;
Cisplatin/*toxicity
;
Creatinine/urine
;
Epithelial Cells/drug effects
;
Erythropoietin/administration & dosage/*therapeutic use
;
Kidney/metabolism
;
Kidney Failure, Acute/*chemically induced/*drug therapy
;
Kidney Tubules/drug effects
;
Male
;
Nordihydroguaiaretic Acid/*therapeutic use
;
Rats
;
Rats, Sprague-Dawley
;
Regeneration