Abstract
Tetramethylpyrazine (TMP), a major active ingredient of Ligusticum wallichi Franchat extract (a Chinese herb), exhibits neuroprotective properties in ischemia. In this study, we assessed its protective effects on Schwann cells (SCs) by culturing them in the presence of oxygen glucose deprivation (OGD) conditions and measuring cell survival in cold ischemic rat nerves. In the OGD-induced ischemic injury model of SCs, we demonstrated that TMP treatment not only reduced OGD-induced cell viability losses, cell death, and apoptosis of SCs in a dose-dependent manner, and inhibited LDH release, but also suppressed OGD-induced downregulation of Bcl-2 and upregulation of Bax and caspase-3, as well as inhibited the consequent activation of caspase-3. In the cold ischemic nerve model, we found that prolonged cold ischemic exposure for four weeks was markedly associated with the absence of SCs, a decrease in cell viability, and apoptosis in preserved nerve segments incubated in University of Wisconsin solution (UWS) alone. However, TMP attenuated nerve segment damage by preserving SCs and antagonizing the decrease in nerve fiber viability and increase in TUNEL-positive cells in a dose-dependent manner. Collectively, our results indicate that TMP not only provides protective effects in an ischemia-like injury model of cultured rat SCs by regulating Bcl-2, Bax, and caspase-3, but also increases cell survival and suppresses apoptosis in the cold ischemic nerve model after prolonged ischemic exposure for four weeks. Therefore, TMP may be a novel and effective therapeutic strategy for preventing peripheral nervous system ischemic diseases and improving peripheral nerve storage.
Highlights
Nerve autografts have remained the gold standard for peripheral nerve gap repair for over 50 years
Ischemic injury can initiate a cascade of events that results in inflammation and cell death by apoptosis and necrosis (Faubel, Edelstein, 2005)
Apoptosis is a type of cell death that occurs as a cascade of cellular machinery
Summary
Nerve autografts have remained the gold standard for peripheral nerve gap repair for over 50 years. Peripheral nerve allograft transplantation requires tissue typing of both the donor and the recipient, and often transportation of graft materials over long distances. These preoperative requirements can result in variable storage times and conditions between the time of harvesting of the graft from the organ donor and implantation into the host. If an optimal storage method can be developed whereby peripheral nerves can be preserved for a sufficient amount of time for transport, nerve allografts would be the first choice in peripheral nerve injury reconstruction. The preservation of peripheral nerve grafts would result in the establishment of a nerve tissue bank
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