What does this research mean for the field?

Isoliensinine improves left ventricular function and reduces cardiomyocyte apoptosis in spontaneous hypertensive rats by activating the PI3K/AKT pathway. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

What question did this study set out to answer?

This research aims to investigate the cardioprotective effects of Isoliensinine and its mechanisms of action.

January 10, 2026Food Science and Human Wellness0 citationsOpen Access

Isoliensinine alleviates cardiac apoptosis by activating the PI3K/AKT Pathway: Insights from in Vivo and in Vitro Studies

MWMeizhu Wu LCLingqi Chen ZGZhi Guo

Key Result

Isoliensinine improved left ventricular function and reduced cardiomyocyte apoptosis in SHR by activating the PI3K/AKT pathway, suggesting its potential as a hypertension therapy.

Key Points

This research aims to investigate the cardioprotective effects of Isoliensinine and its mechanisms of action.
Spontaneous hypertensive rats received Isoliensinine or valsartan for 10 weeks.
Cardiac function, apoptosis, and gene expression were assessed in vivo and in vitro.
Transcriptomic analysis identified changes in gene expression linked to apoptosis and the PI3K/AKT pathway.
Cellular assays were performed to confirm binding interactions of Isoliensinine with PI3K and AKT.
Isoliensinine significantly improved left ventricular function in hypertensive rats.
Decreased cardiomyocyte apoptosis was observed in both in vivo and in vitro settings.
Transcriptomic analysis revealed Isoliensinine reversed multiple regulated transcripts associated with cardiac dysfunction.
Isoliensinine restored PI3K/AKT phosphorylation levels, indicating pathway activation.

Structured PICO

Does Isoliensinine improve cardiac function and reduce cardiomyocyte apoptosis in spontaneous hypertensive rats?

Population

30 Spontaneous hypertensive rats (SHR) and 6 Wistar-Kyoto (WKY) rats, 4-week-old males; and AngII-stimulated H9c2 cardiomyocytes.

Intervention

Isoliensinine (2.5, 5, 10 mg/kg/day by gavage for 10 weeks in vivo; 2.5, 5, 10 μmol/L for 48 h in vitro)

Comparator

Double-distilled water (model control) and Valsartan 10 mg/kg/day (active comparator)

Outcome

Cardiac function (LVEF, LVFS, IVS;d, LVID;d), histopathology, apoptosis, and transcriptomic changessurrogate

Isoliensinine demonstrates cardioprotective effects in hypertensive rats by inhibiting cardiomyocyte apoptosis via the PI3K/AKT signaling pathway.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

This study investigated the cardioprotective effects of Isoliensinine, a bisbenzylisoquinoline alkaloid from Nelumbo nucifera Gaertn, and its underlying mechanisms. Spontaneous hypertensive rats (SHR) received Isoliensinine (2.5, 5, 10 mg/kg/day) or valsartan (10 mg/kg/day) for 10 weeks, with Wistar-Kyoto rats as controls. Cardiac function, histopathology, apoptosis, and transcriptomic changes were evaluated in vivo and in Angtension II (AngII)-stimulated H9c2 cardiomyocytes in vitro. Isoliensinine significantly improved left ventricular function, and ameliorated pathological cardiac damage in SHR. Transcriptomic analysis revealed that Isoliensinine reversed 111 up-regulated and 127 down-regulated transcripts in cardiac tissues of SHR, with enrichment of pathways related to apoptosis and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Both in vivo and in vitro experiments confirmed that Isoliensinine reduced cardiomyocyte apoptosis and restored PI3K/AKT phosphorylation. Cellular thermal shift assay (CETSA) and molecular docking supported potential binding of Isoliensinine to PI3K and AKT. Co-treatment with PI3K/AKT activator 740Y-P did not negate the effects of Isoliensinine, suggesting pathway specificity. These findings indicated that Isoliensinine alleviates hypertensive cardiac dysfunction by inhibiting cardiomyocyte apoptosis primarily through modulation of the PI3K/AKT pathway and may serve as a promising therapeutic agent for hypertension.

Ask AI

Helpful

Bookmark

View Full Paper