ABSTRACT
Escin, as an internally applied anti-inflammatory agent, has been widely used in the treatment of inflammation and edema resulting from trauma or operation in the clinic. However, the effect of its external use on cutaneous inflammation and edema remains unexplored. In the present study, the anti-inflammatory and anti-edematous effects of external use of escin were studied in carrageenan-induced paw edema and histamine-induced capillary permeability in rats, paraxylene-induced ear swelling in mice, and cotton pellet-induced granuloma in rats. Effects of external use of escin gel on prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were determined by ELISA. The anti-inflammatory mechanism was explored by detecting the expression of glucocorticoid receptor (GR) with Western blotting and Real-time PCR analyses, with further exploration of nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (P38MAPK) and activator protein-1 (AP-1) expressions. We demonstrated that external use of escin showed significant anti-inflammatory effects on acute and chronic inflammation in different animal models and its anti-inflammatory effects might be related to down-regulation of PGE2, TNF-α, and IL-1β. The results also showed that escin exerted its anti-inflammatory effects by promoting the expression of GR, with the possible mechanism being inhibition of the expressions of GR-related signaling molecules such as NF-κB and AP-1.
Subject(s)
Animals , Female , Humans , Male , Mice , Rats , Aesculus , Chemistry , Anti-Inflammatory Agents , Dinoprostone , Allergy and Immunology , Edema , Drug Therapy , Genetics , Allergy and Immunology , Escin , Interleukin-1beta , Genetics , Allergy and Immunology , Plant Extracts , Rats, Sprague-Dawley , Receptors, Glucocorticoid , Genetics , Allergy and Immunology , Tumor Necrosis Factor-alpha , Genetics , Allergy and ImmunologyABSTRACT
Escin, as an internally applied anti-inflammatory agent, has been widely used in the treatment of inflammation and edema resulting from trauma or operation in the clinic. However, the effect of its external use on cutaneous inflammation and edema remains unexplored. In the present study, the anti-inflammatory and anti-edematous effects of external use of escin were studied in carrageenan-induced paw edema and histamine-induced capillary permeability in rats, paraxylene-induced ear swelling in mice, and cotton pellet-induced granuloma in rats. Effects of external use of escin gel on prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were determined by ELISA. The anti-inflammatory mechanism was explored by detecting the expression of glucocorticoid receptor (GR) with Western blotting and Real-time PCR analyses, with further exploration of nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (P38MAPK) and activator protein-1 (AP-1) expressions. We demonstrated that external use of escin showed significant anti-inflammatory effects on acute and chronic inflammation in different animal models and its anti-inflammatory effects might be related to down-regulation of PGE2, TNF-α, and IL-1β. The results also showed that escin exerted its anti-inflammatory effects by promoting the expression of GR, with the possible mechanism being inhibition of the expressions of GR-related signaling molecules such as NF-κB and AP-1.
Subject(s)
Animals , Female , Humans , Male , Mice , Rats , Aesculus , Chemistry , Anti-Inflammatory Agents , Dinoprostone , Allergy and Immunology , Edema , Drug Therapy , Genetics , Allergy and Immunology , Escin , Interleukin-1beta , Genetics , Allergy and Immunology , Plant Extracts , Rats, Sprague-Dawley , Receptors, Glucocorticoid , Genetics , Allergy and Immunology , Tumor Necrosis Factor-alpha , Genetics , Allergy and ImmunologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between trans, trans-muconic acid (ttMA) as benzene metabolite of occupational workers and benzene concentration in air.</p><p><b>METHODS</b>A rapid and sensitive high-performance liquid chromatography was developed to determine the level of urinary ttMA. ttMA was extrated from urinary samples in liquid-liquid phase a ODS (2) (5u) column (phi 4.6 mm x 150 mm) and detected at wavelength 264 nm in a UV detector using vanillic acid as an internal standard. The mobile phase was acetaticacid/tetrahydrofuran/methanol/water (v/v, 1:2:10:87). The method was validated with 56 urine samples collected from occupationally benzene-exposed individuals.</p><p><b>RESULTS</b>A correlation coefficient (r = 0.9963) was found for ttMA ranging 0.10-10.00 microg/mL. The limit of detection was 0.10 microg/mL. The recovery and reproducibility were generally over 90%. There was a positive correlation between ttMA and benzene level in air. The equation was Y = 0.859 + 0.108C (before work, r = 0.6200) or Y = 1.980 + 0.179C (after work, r = 0.7930).</p><p><b>CONCLUSION</b>This method can be used to determine and control the level of urinary ttMA in those who are occupationally exposed to benzene.</p>
Subject(s)
Humans , Air Pollutants, Occupational , Urine , Benzene , Metabolism , Biomarkers , Urine , Calibration , Chromatography, High Pressure Liquid , Methods , Environmental Monitoring , Methods , Metallurgy , Occupational Exposure , Reproducibility of Results , Sorbic AcidABSTRACT
<p><b>AIM</b>To investigate the protective effects of sodium beta-aescin on cerebral ischemia-reperfusion injury in rats.</p><p><b>METHODS</b>Rats were pretreated with sodium beta-aesein for 7 d and then subjected to cerebral ischemia-reperfusion injury induced by a middle cerebral artery occlusion (MCAO). The neurological outcome was evaluated by the Longa's method; The infarct volume was assessed by hemmatoxylin-Eosin staining and the cerebral water content was measured by dry weight method. The activities of SOD, GSH-Px, CAT, Na+ -K+ -ATPase and the MDA content were measured in the cortex and hippocampus of ischemic and non-ischemic hemisphere.</p><p><b>RESULTS</b>Sodium beta-aescin significantly reduced the volume of cerebral infarct and water content, and ameliorated the neurological deficit (P < 0.05). In vehicle-treated rats, the activities of SOD, GSH-Px and Na+ -K+ -ATPase in the cortex and hippocampus of ischemic hemisphere were all decreased (P < 0.01) , while the CAT activity was slightly elevated and the MDA of content was significantly increased (P < 0.01) compared with the sham-operated group. After treated with sodium beta-aescin, the effects on recovery of SOD, GSH-Px, Na+ -K+ -ATPase activities were observed (P < 0.05), and the MDA content was reduced (P < 0.05).</p><p><b>CONCLUSION</b>These results showed that pretreatment with sodium beta-aescin can attenuate brain injury and its antioxidant activity on rats which encountered cerebral ischemia-reperfusion.</p>