Figure 1.

Taurine could attenuate the enhanced proteasomal degradation of TonEBP under ischemia both in vivo and in vitro. The ischemia could promote the posttranscriptional degradation of TonEBP, as the mRNA level of TonEBP did not change in vitro or in vivo (a, N=4); the protein level, however, decreased significantly (b and c, N=4). The supplementation of taurine could not affect the expression level of TonEBP mRNA (a), but could ameliorate the ischemia-induced degradation of TonEBP (b and c). The following mechanism study supported proteasomal degradation involved under ischemic insults (d–f), as the protein degraded gradually with protein synthesis inhibited by CHX (d, N=3), and the proteasome inhibitor, MG-132, could inhibit such degradation (e, N=3). Furthermore, taurine could inhibit the activation of ubiquitin-proteasomal degradation of TonEBP (f, N=3). Therefore, we confirm that taurine could attenuate the posttranscriptional degradation of TonEBP by inhibiting the ubiquitin-proteasomal pathway. Staining for RFL-32 was performed to indicate approximate equal loading of samples. (Data were expressed as mean±S.E.M. **P<0.01; CHX, cycloheximide; CTL, control; NS, no significance; LAD, left anterior descending coronary artery ligation; OGD, oxygen glucose deprivation; Tau, taurine)