Tags

Type your tag names separated by a space and hit enter

Ginsenoside Rg1 suppressed inflammation and neuron apoptosis by activating PPARγ/HO-1 in hippocampus in rat model of cerebral ischemia-reperfusion injury.
Int J Clin Exp Pathol. 2015; 8(3):2484-94.IJ

Abstract

Generally accepted, inflammation and neuron apoptosis are two characterized pathological features of cerebral ischemia-reperfusion (IR) injury. Ginsenoside Rg1 was reported showing distinct neuroprotective effect in cerebral IR injury but the underlying mechanisms are still unclear. PPARγ/Heme oxygenase-1 (HO-1) signaling was proved effective in suppressing both apoptosis and inflammation. This study was aimed to investigate whether PPARγ/HO-1 signaling was involved in cerebral IR injury and ginsenoside Rg1's neuroprotective effect in cerebral IR injury. Cerebral IR injury was induced by middle cerebral artery occlusion in rats. The PPARγ agonist rosiglitazone (ROZ) and the HO-1 inhibitor zinc protoporphyrin-IX (ZnPP) and ginsenoside Rg1 at various concentrations were used to treat the modeled rats. Neurological deficits, apoptosis and inflammation in hippocampus were evaluated. Furthermore, HO-1 enzymatic activity, expression levels of apoptosis-related and inflammation-related proteins, concentrations of inflammatory cytokines were also determined. The results showed that PPARγ activation by ROZ significantly attenuated neurological deficits, apoptosis and inflammation in hippocampus in cerebral IR rats. However, the neuroprotective effect of ROZ was then impaired by HO-1 inhibitor ZnPP. This effect was evidenced by changes of expression levels of PPARγ, bcl-2, cleaved caspase-3, cleaved caspase-9, IL-1β, TNF-α, HMGB1, and RAGE in hippocampus of modeled animals. Ginsenoside Rg1 showed similar effect to ROZ in activating PPARγ/HO-1 in protecting against apoptosis and inflammation but also impaired by ZnPP administration. In conclusion, PPARγ/HO-1 signaling was critical in mediating apoptosis and inflammation, which was also the therapeutic target of ginsenoside Rg1 in cerebral IR injury.

Authors+Show Affiliations

Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.Department of Anesthesia, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China ; Department of Surgery, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26045754

Citation

Yang, Yuandong, et al. "Ginsenoside Rg1 Suppressed Inflammation and Neuron Apoptosis By Activating PPARγ/HO-1 in Hippocampus in Rat Model of Cerebral Ischemia-reperfusion Injury." International Journal of Clinical and Experimental Pathology, vol. 8, no. 3, 2015, pp. 2484-94.
Yang Y, Li X, Zhang L, et al. Ginsenoside Rg1 suppressed inflammation and neuron apoptosis by activating PPARγ/HO-1 in hippocampus in rat model of cerebral ischemia-reperfusion injury. Int J Clin Exp Pathol. 2015;8(3):2484-94.
Yang, Y., Li, X., Zhang, L., Liu, L., Jing, G., & Cai, H. (2015). Ginsenoside Rg1 suppressed inflammation and neuron apoptosis by activating PPARγ/HO-1 in hippocampus in rat model of cerebral ischemia-reperfusion injury. International Journal of Clinical and Experimental Pathology, 8(3), 2484-94.
Yang Y, et al. Ginsenoside Rg1 Suppressed Inflammation and Neuron Apoptosis By Activating PPARγ/HO-1 in Hippocampus in Rat Model of Cerebral Ischemia-reperfusion Injury. Int J Clin Exp Pathol. 2015;8(3):2484-94. PubMed PMID: 26045754.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Rg1 suppressed inflammation and neuron apoptosis by activating PPARγ/HO-1 in hippocampus in rat model of cerebral ischemia-reperfusion injury. AU - Yang,Yuandong, AU - Li,Xin, AU - Zhang,Lingmin, AU - Liu,Lin, AU - Jing,Guixia, AU - Cai,Hui, Y1 - 2015/03/01/ PY - 2015/01/01/received PY - 2015/02/25/accepted PY - 2015/6/6/entrez PY - 2015/6/6/pubmed PY - 2016/3/24/medline KW - Cerebral ischemia-reperfusion injury KW - PPARγ KW - apoptosis KW - inflammation SP - 2484 EP - 94 JF - International journal of clinical and experimental pathology JO - Int J Clin Exp Pathol VL - 8 IS - 3 N2 - Generally accepted, inflammation and neuron apoptosis are two characterized pathological features of cerebral ischemia-reperfusion (IR) injury. Ginsenoside Rg1 was reported showing distinct neuroprotective effect in cerebral IR injury but the underlying mechanisms are still unclear. PPARγ/Heme oxygenase-1 (HO-1) signaling was proved effective in suppressing both apoptosis and inflammation. This study was aimed to investigate whether PPARγ/HO-1 signaling was involved in cerebral IR injury and ginsenoside Rg1's neuroprotective effect in cerebral IR injury. Cerebral IR injury was induced by middle cerebral artery occlusion in rats. The PPARγ agonist rosiglitazone (ROZ) and the HO-1 inhibitor zinc protoporphyrin-IX (ZnPP) and ginsenoside Rg1 at various concentrations were used to treat the modeled rats. Neurological deficits, apoptosis and inflammation in hippocampus were evaluated. Furthermore, HO-1 enzymatic activity, expression levels of apoptosis-related and inflammation-related proteins, concentrations of inflammatory cytokines were also determined. The results showed that PPARγ activation by ROZ significantly attenuated neurological deficits, apoptosis and inflammation in hippocampus in cerebral IR rats. However, the neuroprotective effect of ROZ was then impaired by HO-1 inhibitor ZnPP. This effect was evidenced by changes of expression levels of PPARγ, bcl-2, cleaved caspase-3, cleaved caspase-9, IL-1β, TNF-α, HMGB1, and RAGE in hippocampus of modeled animals. Ginsenoside Rg1 showed similar effect to ROZ in activating PPARγ/HO-1 in protecting against apoptosis and inflammation but also impaired by ZnPP administration. In conclusion, PPARγ/HO-1 signaling was critical in mediating apoptosis and inflammation, which was also the therapeutic target of ginsenoside Rg1 in cerebral IR injury. SN - 1936-2625 UR - https://www.unboundmedicine.com/medline/citation/26045754/Ginsenoside_Rg1_suppressed_inflammation_and_neuron_apoptosis_by_activating_PPARγ/HO_1_in_hippocampus_in_rat_model_of_cerebral_ischemia_reperfusion_injury_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/26045754/ DB - PRIME DP - Unbound Medicine ER -