Objective The present study evaluated the antinociceptive activity of Calendula officinalis L.(Ca)cream on inflammatory *** Creams with different Ca concentrations were tested for their ability to ameliorate pain-rela...
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Objective The present study evaluated the antinociceptive activity of Calendula officinalis L.(Ca)cream on inflammatory *** Creams with different Ca concentrations were tested for their ability to ameliorate pain-related behavior and edema in rats using formalin test,carrageenan(Cg)-induced acute inflammation model,bradykinin(BK)-induced acute inflammation model,and complete Freund’s adjuvant(CFA)-induced chronic inflammation *** the formalin test,we also examined the implication of peripheral opioid receptors in the antinociceptive mechanisms of Ca cream,by means of Q-naloxone,a peripherally acting nonselective opioid ***,the effects of Ca cream compared with diclofenac on BK-induced edema were examined when the kininase II in tissue was preserved or inhibited by *** local production of redox biomarkers in formalin model,tumor necrosis factor-α(TNF-α)in Cg model and histopathological changes in CFA model were also *** A single application of Ca cream at a dose of 10%or 30%(w/w)decreased the formalin-induced licking/biting behavior during both phases of this test in a Q-naloxone-sensitive *** effect was associated with the reduction of oxidative stress in the injured paw and the edema associated with the later phase of formalin-induced pain.A single application of Ca cream(10%or 30%)reduced paw edema and thermal hypernociception in Cg-induced acute inflammation,corresponding with a local decrease in TNF-α.Ca cream also inhibited BK-induced spontaneous nociceptive behavior and paw inflammation in both paradigms *** applications of Ca cream also decreased CFA-induced chronic inflammation,mechanical hypernociception and histopathological changes in the *** These results reveal the topical antinociceptive and antiedematogenic effects of Ca cream.A modulatory action on peripheral opioid receptors associated with its antioxidant mechanism may be involved,at least in par
AIM: To validate whether the platelet count/spleen size ratio can be used to predict the presence of esophageal varices in Mexican patients with hepatic cirrhosis.
AIM: To validate whether the platelet count/spleen size ratio can be used to predict the presence of esophageal varices in Mexican patients with hepatic cirrhosis.
Oxidative stress has been involved in neurodegenerative diseases. The growth hormone (GH) counteracts the levels of reactive oxygen species. Previously, we showed that the prolonged exposure to ozone causes oxidative ...
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Oxidative stress has been involved in neurodegenerative diseases. The growth hormone (GH) counteracts the levels of reactive oxygen species. Previously, we showed that the prolonged exposure to ozone causes oxidative stress in the hippocampus and memory deficits. In this work, we analyzed the effects of the growth hormone on the memory deficit generated by ozone exposure, growth hormone effects on the Insulin-like growth factor I (IGF-I), and the serinethreonine protein kinase (Akt) activation in the dentate gyrus. Our results show that GH prevents memory deficits in early stages of the neurodegenerative process.
Chronic exposure to low doses of ozone similar to a day of high pollution in Mexico City causes a state of oxidative stress. This produces a progressive neurodegeneration in hippocampus of rats exposed to the gas. The...
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Chronic exposure to low doses of ozone similar to a day of high pollution in Mexico City causes a state of oxidative stress. This produces a progressive neurodegeneration in hippocampus of rats exposed to the gas. The aim of this study was to analyze the effect of chronic exposure on the changes in the blood-brain barrier in rats exposed to low doses of ozone. Method: each group received one of the following treatments, control group received air without ozone, and groups 2, 3, 4, 5, and 6 received ozone doses of 0.25 ppm for 4 h daily during 7, 15, 30, 60 and 90 days respectively. Each group was processed to inmunohistochemical technique against of the following antibody: blood-brain barrier, guanylyl cyclase, Iba-1, GFAP, NFκ-B, TNF-α. The results show that there is a correlation between the time exposure of ozone and the progressive damage, on the blood-brain barrier rupture, finally causing edema of endothelial cell, increase in guanylyl cyclase type 1, thickening of the processes and astrocytes foot, and an increase in the expression of factors NFκ-B and TNF-α at 30 and 60 days of exposure to this gas. All the above indicates that the chronic state of oxidative stress causes a neurodegeneration process, accompanied by disruption of the blood-brain barrier likely to occur in the Alzheimer’s disease.
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