1.Methods of bone marrow mesenchymal stem cells differentiating into hepatocytes and the underlying mechanisms
Shucai XIE ; Jianquan ZHANG ; Xili JIANG ; Shuai ZHOU
Chinese Journal of Tissue Engineering Research 2016;20(50):7586-7593
BACKGROUND:A number of studies have shown that there are many inducible methods by which bone marrow mesenchymal stem cel s can differentiate into hepatocytes, but the specific molecular mechanism is unclear yet. OBJECTIVE:To review the programs and underlying mechanisms by which bone marrow mesenchymal stem cel s differentiate into hepatocytes. METHODS:A computer-based online search of CNKI, VIP, WanFang and PubMed databases was performed to retrieve articles about directional differentiation of bone marrow mesenchymal stem cel s into hepatocytes published between 2004 and 2015. The key words were“hepatocyte (-like) cel s, bone marrow mesenchymal stem cel s, differentiation”in Chinese and English, respectively. Final y, 62 articles were included in result analysis. RESULTS AND CONCLUSION:There are many programs for hepatic differentiation of bone marrow mesenchymal stem cel s, but the specific molecular mechanism is stil unclear. Many studies mainly focus on Notch signaling pathway, Wnt/β-catenin signaling pathway, P38 signal pathway, miR-122 and effect of calcium ions. Bone marrow mesenchymal stem cel s that can be induced to differentiate into mature hepatocytes provide an ideal cel ular source for hepatocyte transplantation and artificial liver, which is proposed to be a new strategy for clinical treatment of end-stage liver disease.
2.Protective effect and mechanism of saponins from Gleditsia sinensis on ischemic stroke with phlegm and blood stasis model rats
Nana DONG ; Xiaolan CHEN ; Bili DENG ; Jing WAN ; Shucai XIE ; Juan HU ; Chenyue LUO ; Guoqiong CAO
China Pharmacy 2022;33(9):1068-1074
OB JECTIVE To study the protective effects of saponins from Gleditsia sinensis on ischemic stroke with phlegm and blood stasis (ISPBS)model rats ,and to explore its mechanism. METHODS Totally 119 rats were randomly divided into normal group (normal saline ),sham operation group (normal saline ),model group (normal saline ),nimodipine group (positive control group ,5 mg/kg),G. sinensis saponin low-dose ,medium-dose and high-dose groups (3.21,6.42 and 12.84 mg/kg),with 17 rats in each group. Except for normal group ,other groups were all given high-fat diet+suture-occluded method to induce ISPBS model. The neurological function score ,water content of brain tissue ,pathological morphology of brain tissue ,the changes of hemorheology indexes (whole blood viscosity , erythrocyte aggregation index , Casson-viscosity), four items of blood lipid [triacylglycerol (TG),total cholesterol (TC),low-density lipoprotein cholesterol (LDL-C),high-density lipoprotein cholesterol(HDL-C)] and inflammatory factors in serum and oxidative stress indexes [malondialdehyde (MDA),nitric oxide (NO),superoxide dismutase (SOD)] in brain tissue were determined or observed in rats. The protein expressions of B lymphocytoma 2(Bcl-2),Bcl-2 associated X protein (Bax)and caspase- 3 in cerebral tissue were also detected. RESULTS Compared with normal group ,the score of nerve function ,5 kinds of serum indexes (TC,TG,LDL-C,TNF-α,IL-1β), hemorheology indexes ,the contents of MDA and NO and protein expressions of Bax and caspase- 3 in cerebral tissue were all increased significantly in model group (P<0.01). The levels of HDL-C and IL- 10 in serum ,SOD activity and protein expression of Bcl- 2 in cerebral tissue were decreased significantly (P<0.01),and obvious lesions such as nuclear pyknosis and cell membrane fragmentation occurred in brain tissue. Compared with model group ,above indexes of administration groups were improved to different extents ,among which there was statistical significance in above indexes of G. sinensis saponin high-dose group (P< 0.01). CONCLUSIONS Saponin from G. sinensis has a good protective effect on ISPBS model rats. Its mechanism may beassociated with reducing oxidative damage , reducing the production of pro-inflammatory mediators and resisting neuronal apoptosis.