从肝肾同源理论的应用出发,结合骨保护素(osteoprotegerin,OPG)/核因子受体活化因子NF-κB配体(receptor activator of NF-κB ligand,RANKL)/NF-κB受体活化因子(receptor activator for NF-κB,RANK)信号系统在骨代谢中的调控机制,阐...从肝肾同源理论的应用出发,结合骨保护素(osteoprotegerin,OPG)/核因子受体活化因子NF-κB配体(receptor activator of NF-κB ligand,RANKL)/NF-κB受体活化因子(receptor activator for NF-κB,RANK)信号系统在骨代谢中的调控机制,阐释肝肾同源理论应用于临床的客观分子生物学依据,更好地指导临床。展开更多
Objective:The objective of this study was to investigate the alterations and potential implications of the Osteoprotegerin(OPG)/Receptor Activator of Nuclear Factor-kappa B Ligand(RANKL)/Receptor Activator of Nuclear ...Objective:The objective of this study was to investigate the alterations and potential implications of the Osteoprotegerin(OPG)/Receptor Activator of Nuclear Factor-kappa B Ligand(RANKL)/Receptor Activator of Nuclear Factor-kappa B(RANK)signaling pathway factors in a murine model of sepsis-associated acute kidney injury(SA-AKI).This research aimed to offer novel insights into the mechanistic exploration of SA-AKI.Methods:The SA-AKI model group(CLP group)was established through cecal ligation and puncture surgery(CLP),while the control group consisted of sham-operated animals(Sham group)subjected only to laparotomy without cecal ligation and puncture.Blood samples were collected 24 h post-surgery,and murine kidney tissues were harvested upon euthanasia.Serum levels of Serum Creatinine(Scr)and Blood Urea Nitrogen(BUN)were quantified using assay kits.Furthermore,serum levels of interleukin-6(IL-6),tumor necrosis factor-alpha(TNF-α),and interleukin-1 beta(IL-1β)were assessed through enzyme-linked immunosorbent assay(ELISA).Renal tissue pathological alterations were examined employing hematoxylin-eosin staining(HE),and the mRNA and protein levels of OPG,RANKL,and RANK in murine kidney tissues were determined via reverse transcription-quantitative polymerase chain reaction(RT-qPCR)and Western blotting.Results:Comparative analysis revealed that,in comparison to the Sham group,the CLP group demonstrated a significant elevation in the levels of Scr,BUN,IL-6,TNF-α,and IL-1β,with statistically significant disparities(all P<0.05).Histopathological examination of the CLP group's kidneys unveiled glomerular congestion,edema,partial ischemic wrinkling,enlargement of interstitial spaces,the presence of necrotic epithelial cells in select renal tubules,tubular luminal dilation,varying degrees of interstitial edema,and infiltration by a limited number of inflammatory cells.In parallel,relative to the Sham group,the CLP group exhibited substantial upregulation in mRNA expression of OPG and RANK in renal tissues,while RANKL mRNA expression experienced marked downregulation,with statistically significant distinctions(all P<0.05).Moreover,in comparison with the Sham group,the CLP group demonstrated an elevation in protein expression of OPG and RANK in kidney tissues,whereas RANKL protein expression displayed significant downregulation,with statistically significant differences(all P<0.05).Conclusion:In a murine sepsis model,augmented expression of OPG and RANK,coupled with diminished RANKL expression,suggests the potential involvement of the OPG/RANKL/RANK signaling pathway in the pathophysiological progression of SA-AKI.展开更多
目的考察白芦藜醇(Resveratrol,RSV)对牙周炎大鼠骨保护素(osteoprotegerin,OPG)/核因子-κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)/核因子-κB受体活化因子(receptor activator of NF-κB,RANK)(OPG/RANKL/RANK...目的考察白芦藜醇(Resveratrol,RSV)对牙周炎大鼠骨保护素(osteoprotegerin,OPG)/核因子-κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)/核因子-κB受体活化因子(receptor activator of NF-κB,RANK)(OPG/RANKL/RANK)信号通路相关蛋白的影响。方法采用不同浓度的RSV对牙周炎大鼠进行干预,采用RT-PCR和Western blot分别检测牙周组织细胞OPG、RANKL、IL-1、IL-6、TNF-α和基质金属蛋白酶8(matrix metalloproteinase 8,MMP-8)的mRNA水平和蛋白表达水平。结果牙周炎模型组大鼠牙周组织中OPG、RANKL、IL-1、IL-6、TNF-α和MMP-8的mRNA表达强度和蛋白水平高于空白对照组(P<0.05),RSV低剂量组、RSV中剂量组、RSV高剂量组则依次低于牙周炎模型组(P<0.05)。结论RSV可以降低牙周炎大鼠牙周组织中OPG、RANKL、IL-1、IL-6、TNF-α和MMP-8的mRNA和蛋白表达水平,改善大鼠牙周组织状况。展开更多
文摘从肝肾同源理论的应用出发,结合骨保护素(osteoprotegerin,OPG)/核因子受体活化因子NF-κB配体(receptor activator of NF-κB ligand,RANKL)/NF-κB受体活化因子(receptor activator for NF-κB,RANK)信号系统在骨代谢中的调控机制,阐释肝肾同源理论应用于临床的客观分子生物学依据,更好地指导临床。
基金Natural Science Foundation of Xinjiang Uygur Autonomous Region(No.2022D01C604)。
文摘Objective:The objective of this study was to investigate the alterations and potential implications of the Osteoprotegerin(OPG)/Receptor Activator of Nuclear Factor-kappa B Ligand(RANKL)/Receptor Activator of Nuclear Factor-kappa B(RANK)signaling pathway factors in a murine model of sepsis-associated acute kidney injury(SA-AKI).This research aimed to offer novel insights into the mechanistic exploration of SA-AKI.Methods:The SA-AKI model group(CLP group)was established through cecal ligation and puncture surgery(CLP),while the control group consisted of sham-operated animals(Sham group)subjected only to laparotomy without cecal ligation and puncture.Blood samples were collected 24 h post-surgery,and murine kidney tissues were harvested upon euthanasia.Serum levels of Serum Creatinine(Scr)and Blood Urea Nitrogen(BUN)were quantified using assay kits.Furthermore,serum levels of interleukin-6(IL-6),tumor necrosis factor-alpha(TNF-α),and interleukin-1 beta(IL-1β)were assessed through enzyme-linked immunosorbent assay(ELISA).Renal tissue pathological alterations were examined employing hematoxylin-eosin staining(HE),and the mRNA and protein levels of OPG,RANKL,and RANK in murine kidney tissues were determined via reverse transcription-quantitative polymerase chain reaction(RT-qPCR)and Western blotting.Results:Comparative analysis revealed that,in comparison to the Sham group,the CLP group demonstrated a significant elevation in the levels of Scr,BUN,IL-6,TNF-α,and IL-1β,with statistically significant disparities(all P<0.05).Histopathological examination of the CLP group's kidneys unveiled glomerular congestion,edema,partial ischemic wrinkling,enlargement of interstitial spaces,the presence of necrotic epithelial cells in select renal tubules,tubular luminal dilation,varying degrees of interstitial edema,and infiltration by a limited number of inflammatory cells.In parallel,relative to the Sham group,the CLP group exhibited substantial upregulation in mRNA expression of OPG and RANK in renal tissues,while RANKL mRNA expression experienced marked downregulation,with statistically significant distinctions(all P<0.05).Moreover,in comparison with the Sham group,the CLP group demonstrated an elevation in protein expression of OPG and RANK in kidney tissues,whereas RANKL protein expression displayed significant downregulation,with statistically significant differences(all P<0.05).Conclusion:In a murine sepsis model,augmented expression of OPG and RANK,coupled with diminished RANKL expression,suggests the potential involvement of the OPG/RANKL/RANK signaling pathway in the pathophysiological progression of SA-AKI.
