Pharmacology
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Using a new animal model of postoperative pain we recently developed, we investigated whether the selective cyclooxygenase-2 (COX-2) inhibitor parecoxib sodium, and the analgesic tramadol hydrochloride, attenuated mechanical primary hyperalgesia induced by minor surgery on the rat tail. ⋯ We have shown that the hyperalgesia in our model of postoperative pain is responsive to treatment with the analgesic tramadol, but it is not responsive to the selective COX-2 inhibitor parecoxib at the doses we used.
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Two groups of rats were used to examine the effect of pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, on rat hearts using an in vivo model of ischemia-reperfusion (I/R) to elucidate potential mechanisms. One group was the 30-min reperfusion group, which was further subdivided into sham (n=5), vehicle (n=6) and pioglitazone (3 mg x kg(-1), n=7) treatment groups with 30 min ischemia followed by 30 min reperfusion to detect data related to cardiac function and the area of myocardial infarction. The other group was the 120-min reperfusion group, subdivided into sham (n=5), vehicle (n=6), and pioglitazone 0.3 mg x kg(-1) (n=6), 1 mg x kg(-1) (n=7) and 3 mg x kg(-1) (n=6) treatment groups. ⋯ In addition, acute treatment with pioglitazone dose-dependently increased PPARgamma expression and decreased MMP-2 expression at protein and mRNA levels. Our findings demonstrate that a PPARgamma agonist may protect the heart from I/R injury. The protective effect is likely to occur by reducing cardiomyocyte apoptosis and inhibiting MMP-2.
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The present study evaluated the role of ventrolateral periaqueductal gray (vlPAG)-located orphanin-FQ (OFQ) in the opioid tolerance induced by repeated microinjections of morphine (MOR) into vlPAG. Microinjection of MOR (5 microg/0.5 microl) into vlPAG caused antinociception as quantified with the tail flick and the hot plate tests. When MOR microinjection was repeated twice daily, the antinociceptive effect disappeared within 2 days (tolerance). ⋯ Furthermore, if OFQ (1 ng/0.5 microl) was microinjected into vlPAG, then a MOR microinjection administered 15 min later into vlPAG did not elicit antinociception. Finally, opioid tolerance induced by repeated systemic MOR injections (5 mg/kg, i.p.) was reversed by a single microinjection of NST into vlPAG. This emphasizes the central importance of vlPAG-located OFQ in the MOR tolerance.
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To evaluate the protective effect of alpha-lipoic acid in reducing oxidative damage after severe hepatic ischemia/reperfusion (IR) injury. ⋯ Since lipoic acid administration alleviated the I/R-induced liver injury and improved the hepatic structure and function, it seems likely that lipoic acid with its antioxidant and oxidant-scavenging properties may be of potential therapeutic value in protecting the liver against oxidative injury due to ischemia-reperfusion.
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The ovariectomized (OVX) rat, as an established animal model of human osteoporosis, was adopted in the present experiment to study the protective effects of sodium daidzein sulfonate (SDS) on trabecular bone. Six-month-old Sprague-Dawley rats were sham-operated or ovariectomized. Five days later, the OVX rats were randomly assigned to one of three experimental groups and treated for 90 days with vehicle, 17beta-estradiol (E(2)) or SDS. ⋯ In the OVX group, the structure of trabecular plate in the femoral head was absorbed and became progressively thinner or was removed completely, accompanied by enlargement of marrow cavities and amalgamation of two or more marrow cavities. Administration of SDS and E(2 )prevented the change of trabecular bone microarchitecture induced by OVX, increasing the trabecular bone area and trabecular thickness, while decreasing the trabecular separation. These results indicate that SDS administration prevents OVX-induced decrease in BMD and bone mechanical strength, and has a moderate protective effect on the microarchitecture of trabecular bone in aged Sprague-Dawley rats.