What question did this study set out to answer?

The study aims to investigate how Lingguizhugan Decoction (LGZGD) protects against cardiac hypertrophy induced by angiotensin II.

January 25, 2026

Lingguizhugan Decoction Attenuates Angiotensin II-Induced Cardiac Hypertrophy Through the LITAF Signaling Pathway

Key Result

Lingguizhugan Decoction significantly attenuates Ang II-induced cardiac hypertrophy by activating the LITAF pathway and inhibiting the ASK1-JNK/p38 signaling cascade.

Key Points

The study aims to investigate how Lingguizhugan Decoction (LGZGD) protects against cardiac hypertrophy induced by angiotensin II.
Established in vivo cardiac hypertrophy model using continuous Ang II infusion in mice.
Administered LGZGD to evaluate its protective effects through echocardiography and molecular techniques.
Conducted in vitro experiments on H9c2 cardiomyocytes treated with Ang II and LGZGD-containing serum.
Silenced LITAF expression in H9c2 cells using siRNA to confirm its role in the anti-hypertrophy effects.
LGZGD improved cardiac function and reduced cardiomyocyte size.
Downregulated hypertrophic markers and upregulated LITAF protein expression.
Suppressed activation of ASK1, JNK1/2, and p38 MAPK pathways.
LITAF silencing reversed LGZGD's anti-hypertrophic effects, affirming its importance.

Structured PICO

Does Lingguizhugan Decoction attenuate Angiotensin II-induced cardiac hypertrophy in preclinical models?

Population

In vivo mouse model of cardiac hypertrophy established via continuous Angiotensin II (Ang II) infusion, and in vitro H9c2 cardiomyocytes treated with Ang II.

Intervention

Lingguizhugan Decoction (LGZGD) administered in vivo, and LGZGD-containing serum applied in vitro.

Comparator

Untreated Ang II-induced hypertrophy models (implied control).

Outcome

Cardiac function, cardiomyocyte size, hypertrophic markers, and expression/phosphorylation of LITAF, ASK1, JNK1/2, and p38 MAPK.surrogate

Lingguizhugan Decoction attenuates Angiotensin II-induced cardiac hypertrophy by activating the LITAF pathway and inhibiting the ASK1-JNK/p38 signaling cascade in preclinical models.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Objective: Lingguizhugan Decoction (LGZGD), a traditional Chinese herbal prescription with recognized efficacy in heart failure, has an unclear mechanism against cardiac hypertrophy. This study investigated its protective effects against angiotensin II (Ang II)-induced cardiac hypertrophy and the role of the LITAF signaling pathway. Methods: An in vivo mouse model of cardiac hypertrophy was established via continuous Ang II infusion. LGZGD was administered, and its effects on cardiac function, hypertrophy markers, and pathway proteins were evaluated using echocardiography, histopathology, and molecular techniques. In vitro, H9c2 cardiomyocytes were treated with Ang II to induce hypertrophy; LGZGD-containing serum was applied to assess the impacts on cell size, hypertrophic markers, and signaling pathways. LITAF expression in H9c2 cells was silenced via siRNA to validate its role in LGZGD-mediated anti-hypertrophy. Results: LGZGD improved cardiac function, reduced cardiomyocyte size, and downregulated hypertrophic markers. It also upregulated LITAF protein expression and suppressed the phosphorylation of ASK1, JNK1/2, and p38 MAPK. LGZGD-containing serum inhibited Ang IIinduced H9c2 hypertrophy via activating LITAF and inhibiting the ASK1–JNK/p38 pathway. LITAF silencing reversed these anti-hypertrophic effects, confirming its pivotal role in mediating LGZGD's protective action. Discussion: LGZGD alleviates cardiac hypertrophy by activating LITAF and inhibiting the ASK1-JNK/p38 pathway, identifying key therapeutic targets of this formula. These findings advance understanding of LITAF’s non-inflammatory cardiovascular protective roles and provide insights into multi-target strategies for cardiac hypertrophy. Conclusion: LGZGD attenuates Ang II-induced cardiac hypertrophy by activating the LITAF pathway and inhibiting the ASK1-JNK/p38 signaling cascade.

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