Sener Göksel, Sert Gülten, Ozer Sehirli A, Arbak Serap, Uslu Bahar, Gedik Nursal, Ayanoglu-Dulger Gül
Marmara University, School of Pharmacy, Department of Pharmacology, Division of Biochemistry, Tibbiye Cad. 34668 Istanbul, Turkey.
Int Immunopharmacol. 2006 May;6(5):724-32. doi: 10.1016/j.intimp.2005.10.010. Epub 2005 Nov 28.
Pressure ulcers (PU) cause morphological and functional alterations in the skin and visceral organs. In this study we investigated the role of oxidative damage in PUs and the probable beneficial effect of beta-glucan treatment against this damage. beta-glucan is known to have immunomodulatory effects. Experiments were carried on Wistar albino rats. PU was induced by applying magnets over steel plates that were implanted under the skin, to compress the skin and cause ischemia where removing the magnets cause reperfusion of the tissue. Within the first 12 h, rats were subjected to 5 cycles of ischemia/reperfusion (I/R), followed by 12 h ischemia. This protocol was repeated for 3 days. In treatment groups, twice a day during reperfusion periods, beta-glucan was either applied locally (25 mg/kg) as an ointment on skin, or administered orally (50 mg/kg) as a gavage. At the end of the experimental periods, tissue samples (skin, liver, kidney, lung, stomach, and ileum) were taken for the measurement of malondialdehyde (MDA)--an index of lipid peroxidation--and glutathione (GSH)--a key antioxidant--levels. Neutrophil infiltration was evaluated by the measurement of tissue myeloperoxidase activity, while collagen contents were measured for the evaluation of tissue fibrosis. Skin tissues were also examined microscopically. Liver and kidney functions were assayed in serum samples. Local treatment with beta-glucan inhibited the increase in MDA and MPO levels and the decrease in GSH in the skin induced by PU, but was less efficient in preventing the damage in visceral organs. However, systemic treatment prevented the damage in the visceral organs. Significant increases in creatinine, BUN, ALT, AST, LDH and collagen levels in PU group were prevented by beta-glucan treatment. The light microscopic examination exhibited significant degenerative changes in dermis and epidermis in the PU group. Tissue injury was decreased especially in the locally treated group. Thus, supplementing geriatric and neurologically impaired patients with adjuvant therapy of beta-glucan may have some benefits for successful therapy and improving quality of life.
压疮(PU)会导致皮肤和内脏器官出现形态和功能改变。在本研究中,我们调查了氧化损伤在压疮中的作用以及β-葡聚糖治疗对这种损伤可能产生的有益效果。已知β-葡聚糖具有免疫调节作用。实验在Wistar白化大鼠身上进行。通过将磁铁置于植入皮肤下的钢板上以压迫皮肤并导致局部缺血,移除磁铁后会使组织再灌注,从而诱导压疮形成。在最初的12小时内,大鼠经历5个缺血/再灌注(I/R)周期,随后缺血12小时。此方案重复3天。在治疗组中,在再灌注期间,β-葡聚糖每天两次,要么作为软膏局部涂抹于皮肤(25毫克/千克),要么通过灌胃口服(50毫克/千克)。在实验期结束时,采集组织样本(皮肤、肝脏、肾脏、肺、胃和回肠)以测量丙二醛(MDA)——脂质过氧化指标——和谷胱甘肽(GSH)——一种关键抗氧化剂——的水平。通过测量组织髓过氧化物酶活性评估中性粒细胞浸润情况,同时测量胶原蛋白含量以评估组织纤维化程度。还对皮肤组织进行了显微镜检查。在血清样本中检测肝功能和肾功能。β-葡聚糖局部治疗抑制了压疮诱导的皮肤中MDA和MPO水平的升高以及GSH的降低,但在预防内脏器官损伤方面效果较差。然而,全身治疗可预防内脏器官损伤。β-葡聚糖治疗可预防压疮组中肌酐、尿素氮、谷丙转氨酶、谷草转氨酶、乳酸脱氢酶和胶原蛋白水平的显著升高。光学显微镜检查显示压疮组真皮和表皮有明显的退行性变化。组织损伤尤其在局部治疗组有所减轻。因此,用β-葡聚糖辅助治疗补充老年和神经功能受损患者可能对成功治疗和改善生活质量有一些益处。