Curcumin Ameliorates Reserpine-Induced Gastrointestinal Mucosal Lesions Through Inhibiting IκB-α/NF-κB Pathway and Regulating Expression of Vasoactive Intestinal Peptide and Gastrin in Rats.

The objective of our study was to investigate whether curcumin protects against reserpine-induced gastrointestinal mucosal lesions (GMLs) in rats and to explore the mechanism of curcumin's action. Sprague-Dawley rats were randomly divided into four groups: control group, reserpine-treated group, reserpine treatment group with curcumin at high dose (200 mg/kg), and reserpine treatment group with curcumin at low dose (100 mg/kg). Rats in reserpine-treated group were induced by intraperitoneally administered reserpine (0.5 mg/kg) for 28 days. TUNEL staining and hematoxylin and eosin staining were used to evaluate the apoptotic cells and morphologic changes. In addition, to explore the mechanism of curcumin in protecting GMLs, we used serum of experimental rats to assess the level of vasoactive intestinal peptide (VIP), gastrin, interleukin-6, interleukin-10, tumor necrosis factor-α and interferon-γ by ELISA and radioimmunoassay. The protein levels of NF-κB, p-IκB-α, IκB-α, Bcl-2, Bax, and cleaved-caspase-3 were examined by western blot analysis. Data were analyzed with SPSS 19.0 software package. Curcumin treatment prevented tissue damage and cell death in the reserpine-treated rats and effectively decreased inflammatory response and balanced the expression of VIP and gastrin in the reserpine-treated rats. NF-κB, p-IκB-α, Bax, and cleaved-caspase-3 were increased in the reserpine group, but the curcumin high-dose group inhibited them. Curcumin can target the IκB-α/NF-κB pathway to inhibit inflammatory response and regulate the level of VIP and gastrin in reserpine-induced GML rats.

[The genes change of hMSC before and after the differentation into neuron-like cells].

OBJECTIVE: To study the genes change of hMSC before and after differentiation into neuron-like cells. METHODS: hMSC were separated from marrow, cultured and expanded in culture medium. After hMSC being induced to differentiate with Shenqiye, Neuron-specific enolase (MSE), neurofilament (NF), and glial fibrillary acidic protein (GFAP) were detected by immunocytochemistry respectively. Using semi-quantitiative RT-PCR to detect ten genes change in hMSC before and after differentiation. Two genes were used to detect the gene sequence. RESULTS: When treated with the inducer--Shenqiye, hMSC exhibited neuronal phenotype. The expressions of NSE and NF in the neuron-like cells were positive, but the glial astrocyte marker GFAP was not found. hMSC expressed germline, ectodermal, endodermal and mesodermal genes prior to neurogenasis. After differentiation, germline genes did not express, while the expressions of endodermal and mesodermal genes were weakened. Ectodermal and neuronal genes expressed stronger. CONCLUSION: hMSC express multipotentiality, and the neural differentiation comprises quantitative modulation of gene expression rather than simple on-off switching of neural specific genes.

[Experimental research on effect of human mesenchymal stem cells induced by shenqi fuzheng injection in cerebral infarction].

OBJECTIVE: To investigate the effect of shenqi fuzheng injection (SFI) in inducing differentiation of human mesenchymal stem cells (hMSCs) in brain stem and its effect on nervous function in model rats of cerebral infarction. METHODS: Middle cerebral artery occlusion model rats were made, and hMSCs was injected into their brain after being amplified in vitro and incubated with SFI for 0.5 h, then the survival, migration and differentiation of hMSCs in brain stem as well as the change of nervous function in model rats were observed. RESULTS: The post-transplantation reject reaction to hMSCs was low, it could survive as long as 6 weeks or more. No difference in area of infarction was shown before and after transplantation. Immunohistochemical staining showed that hMSCs expressed human neuron specific enolase (NSE), neurofilament (NF) and glial fibrillary acid protein (GFAP). The limb-kinetic function and tactile perception were improved in the model rats. CONCLUSION: SFI can induce hMSCs differentiate into neurons in vivo, and hMSCs may be the ideal germinal cells for treating cerebral infarction.

[Gene reversion of induced differentiation of adult human bone marrow-derived mesenchymal stem cells into neuron-like cells].

OBJECTIVE: To observe gene reversion during differentiation of human adult bone marrow-derived mesenchymal stem cells (MSCs) into neuron-like cells induced by Shenqiye. METHODS: The MSCs were separated, cultured and expanded in the culture medium and induced to differentiate into neuron-like cells with Shenqiye. The expressions of neuron-specific enolase (NSE), neurofilament (NF), and glial fibrillary acidic protein (GFAP) were detected by immunocytochemical method, and the changes of 10 genes of the cells after differentiation were detected by reverse transcriptional PCR. RESULTS: The MSCs exhibited neuronal phenotype when treated with Shenqiye and the neuron-like cells were positive for expressions of NSE and NF but not for glial astrocyte marker GFAP. After withdrawal of Shenqiye from the medium, the neuron-like cells were reversed to MSC, flat or spindal in morphology. The gene expression profiles of the redifferentiated cells were similar to those of undifferentiated MSCs. CONCLUSION: Shenqiye can induce MSC differentiation into neuron-like cells during and after which gene reversion may occur.