ABSTRACT
BACKGROUND: The low success rate of dental implants under oxidative stress is one of the problems that needs to be resolved urgently. Human dental pulp stem cells (HDPSCs) have a high potential for multiplication, self-renewal and multidirectional differentiation. HDPSCs have achieved some success in tissue engineering for repairing tissue defects. However, with the in-depth research on oxidative stress, eliminating the adverse effect of oxidative stress on HDPSCs used in tissue engineering becomes urgent. OBJECTIVE: To review the application progress of HDPSCs in tissue engineering in recent years and to summarize the effects of oxidative stress on HDPSCs. METHODS: Using "dental pulp stem cells; oxidative stress" as the Chinese and English search terms, we retrieved CNKI and PubMed databases for relevant articles published from January 2001 to December 2017, respectively. After initial screening, 50 eligible articles were further detailed, analyzed and summarized. RESULTS AND CONCLUSION: HDPSCs have the potential of multiplication, self-renewal and multidirectional differentiation. Immunoregulatory mechanism of HDPSCs is achieved through sub-secreting soluble factors and cytokines and inhibiting the upregulation of T lymphocytes and regulatory T cells, which leads to immune tolerance. Oxidative stress as an important factor affecting cell survival impedes cell proliferation and differentiation via a variety of signal transduction pathways. Current studies on the application of HDPSCs in tissue engineering and regenerative medicine for tissue defect repair are still in its infancy, and there are many problems concerning its regulatory mechanism. Further determination of the oxidative stress mechanism of HDPSCs is warranted.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of dopamin receptors-2 (DR2) on myocardial ischemic postconditioning and explore its underlying mechanisms.</p><p><b>METHODS</b>The myocardial ischemic postconditioning (PC) model was established in cultured primary rat neonatal cardiomyocytes which were then randomly assigned in the following groups: Nomial control group, Isehemia/reperfusion (L'R) group, PC (ischemic postconditioning) group, PC + Bro (Bromocriptine, a DB2 antagonist) group, PC + Hal (Haloperidol, a DB2 repressor) and PC + Hal + Bro groups. The lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell medium were analyzed by colorunetry. The cell ultrastructure changes were observed by transmission electron microscope. The cell apoptosis was analyzed using flowcytometiy. The protein expression level of D112 and activity of p-p38 and p-JNK were detected by Western blot.</p><p><b>RESULTS</b>Compared with the nonnal control group, hR increased the protein expression level of DB2, enhanced LDH activity and MDA content, promoted cell injury and apoptosis, decreased SOD activity, up-regulated the activity of p-p38 and p-JNK. Compared with the hR group, although PC further increased the expression of DR2 protein, it decreased LDH activity and MDA content, cell injury and apoptosis, increased SOD activity, down-regulated activity of p-p38 and p-JNK. Bromocriptine treatment further enhanced PC-induced canlioprotective effect, yet Hal addition attenuated this enhancing effect exerted by bromocriptine.</p><p><b>CONCLUSION</b>The activation of DB2 is involved in the protective effect of ischemic postconditioning on myocardial ischemia/reperfusion injury through down-regulating the activity of p-p38 and p-JNK.</p>