Key result
Tetrandrine increases post-injury cardiomyocyte viability to ~70%, outperforming fangchinoline in preclinical models.
Why the study?
Does tetrandrine improve cell viability and reduce LDH release in H9C2 cardiomyocytes under hypoxia/reoxygenation injury?
Does tetrandrine improve cell viability and reduce LDH release in H9C2 cardiomyocytes under hypoxia/reoxygenation injury?
Answers are grounded in this paper and cite their sources.
Tetrandrine demonstrates cardioprotective and metabolic benefits in an in vitro model of myocardial ischemia/reperfusion injury.
S. Moore, particularly tetrandrine, show cardioprotective effects in H9C2 cardiomyocytes under hypoxia/reoxygenation (H/R) injury. Using acid-base extraction and thin-layer chromatography (TLC), HPD-100 resin, Sephadex LH-20, preparative liquid chromatography (prep-HPLC), total alkaloids were purified. In H/R-induced injury (cell viability: 33%), tetrandrine significantly improved viability to 70% and reduced Lactate Dehydrogenase (LDH) release (284-136 U/I), outperforming fangchinoline (viability: 48%; LDH: 223 U/I). Tetrandrine also enhanced glucose consumption (0.62-1.66 nM), lactate production (0.2-0.64 nM), and ATP concentration (5-22 nmoL/mg protein), suggesting metabolic protection. These findings highlight tetrandrine's potential in mitigating myocardial ischemia/reperfusion injury.
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Ji et al. (2026) studied Hypoxia/reoxygenation (H/R) injury. Tetrandrine vs. H/R-induced injury control was evaluated on Cell viability. Tetrandrine significantly improved H9C2 cardiomyocyte viability to 70% (vs 33% in H/R injury control) and reduced LDH release, outperforming fangchinoline.
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