The main active components extracted from Panax notoginseng are total saponins. They have been shown to inhibit platelet aggregation, increase cerebral blood flow, improve neurological behavior, decrease infarct volume and promote proliferation and differentiation of neural stem cells in the hippocampus and lateral ventricles. However, there is a lack of studies on whether total saponins of Panax notoginseng have potential benefits on immature neuroblasts in the olfactory bulb following ischemia and reperfusion. This study established a rat model of global cerebral ischemia and reperfusion using four-vessel occlusion. Rats were administered total saponins of Panax notoginseng at 75 mg/kg intraperitoneally 30 minutes after ischemia then once a day, for either 7 or 14 days. Total saponins of Panax notoginseng enhanced the number of doublecortin (DCX)~+ neural progenitor cells and increased co-localization of DCX with neuronal nuclei and phosphorylated cAMP response element-binding/DCX~+ neural progenitor cells in the olfactory bulb at 7 and 14 days post ischemia. These findings indicate that following global brain ischemia/reperfusion, total saponins of Panax notoginseng promote differentiation of DCX~+ cells expressing immature neuroblasts in the olfactory bulb and the underlying mechanism is related to the activation of the signaling pathway of cyclic adenosine monophosphate response element binding protein.
MOLECULAR MEDICINE REPORTS,2015年11(6):4047-4052 ISSN：1791-2997
[Ge, Jin-Wen; Wang, Guo-Zuo] College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China;[Liao, Jun; Shi, Yong-Mei] Department of Anatomy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China;[Xia, Xing] Campus Network Center, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China
[Ge, JW] Hunan Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, 300 Xueshi St, Changsha 410208, Hunan, Peoples R China.
The expression of Ferroportin (Fpn) was examined at different time points in rats following focal cerebral ischemia treated with or without the traditional Chinese medicine Naotaifang. Initially, rats were randomly divided into 2, 6, 12, 24 and 72 h groups following middle cerebral artery occlusion (MCAO) and the mRNA and protein level of Fpn was detected by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) at the above time points. Secondly, the rats were randomly divided into five groups as follows: Sham surgery group, model group, low-dose group (3 g/kg NTE), medium dose group (9 g/kg NTE) and the high-dose group (27 g/kg NTE). After 3 days of corresponding therapy by intragastric administration once a day, the regional cerebral ischemia model was reproduced by the MCAO suture method. On the third day, the neurological behavior of the rats was analyzed by neurobehavioral assessment. Fpn in the hippocampal CA2 region was measured by immunohistochemistry and the mRNA level of Fpn was detected by RT-PCR. Expression of Fpn in the hippocampal CA2 region reached a peak 12 h after surgery (P<0.05, compared with the model group). The high-dose group (27 g/kg NTE) exhibited a lower neurological behavior score (P<0.05) and a higher level of expression of Fpn at the mRNA and protein level compared with the sham surgery group and model group (P<0.05). Dysregulation of intracellular iron balance is possibly a new mechanism underlying cerebral ischemia. NTE can protect the neuronal population in the hippocampal CA2 region by adjusting the expression of Fpn to balance iron levels following cerebral ischemia.
[Ge, Jin-Wen] Hunan Univ Chinese Med, Dept Integrated Chinese & Western Med, Changsha 410208, Hunan, Peoples R China.;[Wang, Shan-Shan] Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Changsha 410208, Hunan, Peoples R China.;[Cheng, Shao-Wu] Hunan Univ Chinese Med, Dept Cytobiol & Mol Biotechnol, Changsha 410208, Hunan, Peoples R China.
Coagulation factor XII (FXII) is a multidomain serine protease that is the starter of intrinsic coagulation pathway. FXII deficiency and clinical hemostasis are not associated with bleeding, so investigators have not considered FXII important in physiology for a long time. In seeking explanation for FXII-independent physiologic hemostasis, investigators found FXII is an essential constitute of contact system that mediates procoagulation and proinflammatory via the intrinsic coagulation pathway or the Kallikrein-kinin system, respectively. Date obtained in infectious inflammation have revealed FXII mediated clotting that limited bacterial or toxin spread in early phases, and regulated fibrinolysis in later. Moreover, FXII mediated two noninfectious inflammation Hereditary angioedema (HAE) and non-specific allergy via bradykinin (BK) formation. In the coagulation, thrombosis not only is involved with coagulation, but is redefined as thrombo-inflammatory disorder. This paper reviews in detail the progresses in roles of FXII intersection between inflammation and coagulation.