PDF(Pubmed)
Abstract：
OBJECTIVE: Diabetic cardiomyopathy (DCM) is a prevalent condition among individuals with diabetes, and is associated with a high mortality rate. The anti-oxidant properties of Jing Huang or Polygonatum sibiricum polysaccharide (PSP) have been extensively used to treat diabetes-related disorders; however, its potential effectiveness against DCM remains unknown. This study aimed to investigate PSP\'s therapeutic effects on DCM in an experimental diabetic mouse model.
METHODS: To induce insulin resistance, mice were fed a high-fat diet for 3 months, followed by intraperitoneal streptozotocin injection to induce slight hyperglycemia and develop DCM. Both DCM and control mice were given PSP orally for 3 weeks. Western blotting was used to detect the protein expressions of protein kinase G, C/EBP homologous protein, glucose-regulated protein 78, phosphodiesterase type 5, protein kinase R-like endoplasmic reticulum (ER) kinase, and phospho-protein kinase R-like endoplasmic reticulum kinase in heart tissue.
RESULTS: The results showed a reduction in bodyweight and blood glucose levels in the PSP therapy group compared with DCM group. PSP also improved cardiac function and had a negligible effect on malondialdehyde activity. Furthermore, the findings showed that PSP alleviated ER and oxidative stress observed in DCM mice hearts, leading to the inhibition of cyclic guanosine monophosphate-specific phosphodiesterase type 5 and cardiac cyclic guanosine monophosphate reactivation. Phosphodiesterase type 5 inhibition reduced high-fat diet-induced cardiac dysfunction and decreased ER stress.
CONCLUSIONS: PSP could effectively protect diabetic myocardium by inhibiting endoplasmic reticulum stress. These findings provide crucial insights into the potential of PSP to ameliorate DCM conditions in diabetic mice by decreasing ER and oxidative stress, and enhancing cyclic guanosine monophosphate protein kinase G signaling.
METHODS: To induce insulin resistance, mice were fed a high-fat diet for 3 months, followed by intraperitoneal streptozotocin injection to induce slight hyperglycemia and develop DCM. Both DCM and control mice were given PSP orally for 3 weeks. Western blotting was used to detect the protein expressions of protein kinase G, C/EBP homologous protein, glucose-regulated protein 78, phosphodiesterase type 5, protein kinase R-like endoplasmic reticulum (ER) kinase, and phospho-protein kinase R-like endoplasmic reticulum kinase in heart tissue.
RESULTS: The results showed a reduction in bodyweight and blood glucose levels in the PSP therapy group compared with DCM group. PSP also improved cardiac function and had a negligible effect on malondialdehyde activity. Furthermore, the findings showed that PSP alleviated ER and oxidative stress observed in DCM mice hearts, leading to the inhibition of cyclic guanosine monophosphate-specific phosphodiesterase type 5 and cardiac cyclic guanosine monophosphate reactivation. Phosphodiesterase type 5 inhibition reduced high-fat diet-induced cardiac dysfunction and decreased ER stress.
CONCLUSIONS: PSP could effectively protect diabetic myocardium by inhibiting endoplasmic reticulum stress. These findings provide crucial insights into the potential of PSP to ameliorate DCM conditions in diabetic mice by decreasing ER and oxidative stress, and enhancing cyclic guanosine monophosphate protein kinase G signaling.
摘要：
目的：糖尿病心肌病（DCM）是糖尿病患者中普遍存在的疾病，并且与高死亡率有关。黄精或黄精多糖（PSP）的抗氧化特性已被广泛用于治疗糖尿病相关疾病；然而，其对DCM的潜在有效性仍然未知。本研究旨在探讨PSP对实验性糖尿病小鼠模型DCM的治疗作用。
方法：诱导胰岛素抵抗，给小鼠喂食3个月的高脂肪饮食，然后腹膜内注射链脲佐菌素诱导轻度高血糖并发展为DCM。DCM和对照小鼠均口服给予PSP3周。蛋白质印迹法检测蛋白激酶G的蛋白表达,C/EBP同源蛋白,葡萄糖调节蛋白78,5型磷酸二酯酶,蛋白激酶R样内质网激酶,和磷酸蛋白激酶R样内质网激酶在心脏组织中的表达。
结果：结果显示，与DCM组相比，PSP治疗组的体重和血糖水平降低。PSP还改善了心脏功能，对丙二醛活性的影响可以忽略不计。此外，结果表明，PSP减轻了DCM小鼠心脏中观察到的ER和氧化应激，导致环磷酸鸟苷特异性磷酸二酯酶5型的抑制和心脏环磷酸鸟苷的再激活。5型磷酸二酯酶抑制减少了高脂饮食诱导的心脏功能障碍并减少了内质网应激。
结论：PSP可通过抑制内质网应激有效保护糖尿病心肌。这些发现为PSP通过降低ER和氧化应激改善糖尿病小鼠DCM状况的潜力提供了重要见解。增强环磷酸鸟苷蛋白激酶G信号传导。
方法：诱导胰岛素抵抗，给小鼠喂食3个月的高脂肪饮食，然后腹膜内注射链脲佐菌素诱导轻度高血糖并发展为DCM。DCM和对照小鼠均口服给予PSP3周。蛋白质印迹法检测蛋白激酶G的蛋白表达,C/EBP同源蛋白,葡萄糖调节蛋白78,5型磷酸二酯酶,蛋白激酶R样内质网激酶,和磷酸蛋白激酶R样内质网激酶在心脏组织中的表达。
结果：结果显示，与DCM组相比，PSP治疗组的体重和血糖水平降低。PSP还改善了心脏功能，对丙二醛活性的影响可以忽略不计。此外，结果表明，PSP减轻了DCM小鼠心脏中观察到的ER和氧化应激，导致环磷酸鸟苷特异性磷酸二酯酶5型的抑制和心脏环磷酸鸟苷的再激活。5型磷酸二酯酶抑制减少了高脂饮食诱导的心脏功能障碍并减少了内质网应激。
结论：PSP可通过抑制内质网应激有效保护糖尿病心肌。这些发现为PSP通过降低ER和氧化应激改善糖尿病小鼠DCM状况的潜力提供了重要见解。增强环磷酸鸟苷蛋白激酶G信号传导。
