Baicalin, a flavonoid glycoside separated from Scutellaria baicalensis, has cardioprotection against ischaemia/reperfusion (I/R) injury. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is considered as an endogenous protective mechanism against I/R injury depending on its anti-oxidant and anti-apoptotic characteristics. The present study demonstrates whether ALDH2 contributes to the cardioprotection of baicalin against hypoxia/reoxygenation (H/R)-inudced H9c2 cardiomyocytes injury. Our results observed that H/R treatment resulted in a significant decrease in cells viability and obvious increases in caspase-3 activity and apoptosis rate in H9c2 cells, while these alterations were evidently reversed by baicalin pretreatment. Simultaneously, baicalin mitigated H/R-induced the decreases in the levels of ALDH2 mRNA and protein as well as the activity of ALDH2 in H9c2 cells. However, we found that daidzin, an ALDH2 antagonist, remarkably attenuated baicalin-elicited inhibitory action on H/R-induced the downregulation of cells viability and Bcl-2 protein expression, and the upregulations of caspase-3 activity, apoptosis rate, cytochrome c and Bax proteins expressions in H9c2 cells. In addition, baicalin reversed H/R-induced oxidative stress as evidenced by the downregulation of malondialdehyde (MAD) and 4-hydroxy aldehydes (4-HNE) levels, the inhibition of endogenous reactive oxygen species (ROS) generation, and the downregulation of superoxide dismutase (SOD) activity induced by H/R treatment, while these effects were also blocked by daidzin. Furthermore, we found that Alda-1, an ALDH2 agonist, also abolished H/R-induced cytotoxicity, apoptosis, and oxidative stress, indicating that ALDH2 mediated H/R-induced H9c2 cell injury. Overall, these results suggested that baicalin prevents H/R-induced apoptosis and oxidative stress through enhancing ALDH activity and expression in H9c2 cardiomyocytes.

Background:We conducted a meta-analysis to assess the efficacy and safety of ketamine for reducing pain and narcotic use for patients undergoing laparoscopic cholecystectomy (LC).Methods:PubMed, Embase, Web of science, Medline, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) were regarded as eligible in our study. After testing the heterogeneity across RCTs, data were aggregated for fixed/random effect model according to the I2 statistic. The meta-analysis was conducted using Stata 11.0 software.Results:Five studies were included, with a total sample size of 212 patients. Current meta-analysis revealed that there were significant differences regarding postoperative pain score at 12 hours [standard mean difference (SMD) = −0.322, 95% confidence interval (95% CI): −0.594 to −0.050, P = .020], 24 hours (SMD = −0.332, 95% CI: −0.605 to −0.059, P = .017), and 48 hours (SMD = −0.340, 95% CI: −0.612 to −0.068, P = .014). Ketamine intervention was found to significantly decrease narcotic use at 12 hours (SMD = −0.296, 95% CI: −0.567 to −0.025, P = .033), 24 hours (SMD = −0.310, 95% CI: −0.581 to −0.039, P = .025), and 48 hours (SMD = −0.338, 95% CI: −0.609 to −0.066, P = .015).Conclusion:Ketamine appeared to significantly reduce postoperative pain and narcotic use following LC. On the basis of the current evidence available, higher quality RCTs are still required for further research.