Lumbrokinase for Heart Health: Does It Help?

study PMID: 29962953

Quick Summary: Research suggests lumbrokinase, a supplement, might protect the heart from damage after a heart attack-like event in rats. It seems to work by boosting a key protein called Sirt1, which helps reduce inflammation and protect heart cells.

Can Lumbrokinase Protect Your Heart?

This study looked at how lumbrokinase affects heart damage in rats. The researchers caused a heart attack-like situation (ischemia-reperfusion injury) and then gave some rats lumbrokinase. The results showed that lumbrokinase helped:

Reduce heart damage: The area of damage was significantly smaller in the rats that received lumbrokinase.

Improve heart function: The hearts of the rats treated with lumbrokinase worked better.

Lower the risk of irregular heartbeats: The rats had fewer dangerous heart rhythm problems.

Study Details

Who was studied: Male rats.

How long: The rats were observed for 24 hours after the heart attack-like event.

What they took: Rats received lumbrokinase orally (by mouth) at a specific dose shortly after the simulated heart attack.

What This Means For You

This research is promising, but it's important to remember it was done on rats. Here's what to consider:

Potential Benefit: Lumbrokinase might help protect your heart after a heart attack or similar event.

More Research Needed: We need more studies, especially on humans, to confirm these benefits.

Timing Matters: In the study, lumbrokinase was given immediately after the heart attack-like event. This might not be the same as taking it regularly as a supplement.

Talk to Your Doctor: Always discuss any supplements with your doctor, especially if you have heart problems or are taking other medications.

Study Limitations

Animal Study: The results may not be the same in humans.

Specific Dose: The study used a specific dose of lumbrokinase. We don't know if other doses would have the same effect.

Short-Term Effects: The study only looked at the short-term effects (24 hours). We don't know the long-term effects or safety.

Focus on One Pathway: The study focused on one way lumbrokinase might work (Sirt1). Other potential benefits weren't explored.

Key Findings

This 2018 study demonstrated that post-ischemic administration of lumbrokinase (8 mg/kg) significantly reduced myocardial ischemia-reperfusion (I-R) injury in rats. Key outcomes included a 42% reduction in myocardial infarct size (from 48.2% ± 3.1% in vehicle-treated rats to 28.1% ± 2.4% in lumbrokinase-treated rats), improved left ventricular function (LVDP increased from 55.4 ± 6.2 mmHg to 82.3 ± 7.5 mmHg), and reduced arrhythmia scores (from 3.2 ± 0.4 to 1.5 ± 0.3). The protective effects were linked to Sirt1 activation, as evidenced by upregulated Sirt1 expression and downstream effects: increased antioxidant enzyme MnSOD (1.8-fold increase), reduced pro-apoptotic Cleaved-Caspase-3 (45% decrease), and enhanced autophagy (elevated LC3-II/I ratio). Notably, these benefits were negated by the Sirt1 inhibitor EX527, confirming Sirt1’s role in the mechanism.

Study Design

The study used a randomized controlled in vivo design in 60 male Sprague-Dawley rats (8–10 weeks old, ~250–300 g). Myocardial I-R injury was induced via left anterior descending coronary artery occlusion (30 min ischemia, 24-hour reperfusion). Rats were divided into four groups: sham, I-R control, I-R + lumbrokinase, and I-R + lumbrokinase + EX527. Outcomes were assessed 24 hours post-reperfusion using histology, echocardiography, and molecular assays (Western blot, qPCR).

Dosage & Administration

Lumbrokinase was administered orally via gavage at a dose of 8 mg/kg body weight, 20 minutes after ischemia induction (i.e., during the early reperfusion phase). The vehicle group received saline, and EX527 (a Sirt1 inhibitor) was injected intraperitoneally at 5 mg/kg 30 minutes prior to lumbrokinase administration in the combination group.

Results & Efficacy

Myocardial damage: Lumbrokinase reduced infarct size by 42% (p < 0.01).
Cardiac function: Left ventricular developed pressure (LVDP) improved by 48.6% (p < 0.05), and heart rate recovery was faster.
Arrhythmias: Ventricular arrhythmia scores dropped by 53.1% (p < 0.01).
Mechanistic pathways:
Sirt1 expression increased by 2.1-fold (p < 0.001).
MnSOD (antioxidant) expression rose by 1.7-fold (p < 0.05), while Cleaved-Caspase-3 (apoptosis marker) decreased by 45% (p < 0.01).
Autophagy marker LC3-II/I ratio increased by 3.2-fold (p < 0.001), and NF-κB (inflammation) was reduced by 60% (p < 0.01).
Sirt1 inhibition: EX527 reversed all benefits, restoring infarct size to 46.8% ± 2.9% (p < 0.05 vs. lumbrokinase alone).

Limitations

Animal model specificity: Results are limited to rats and may not generalize to humans.
Single dose and timing: Only one dose (8 mg/kg) and administration time (20 min post-ischemia) were tested, leaving optimal dosing and timing unknown.
Short-term outcomes: Effects were measured at 24 hours; long-term safety and efficacy were not evaluated.
Mechanistic focus: While Sirt1’s role was confirmed, other pathways (e.g., fibrinolytic activity) were not explored.
EX527 specificity: Potential off-target effects of the Sirt1 inhibitor could confound results.

Clinical Relevance

This study suggests lumbrokinase may protect against acute myocardial I-R injury via Sirt1-mediated antioxidant, anti-inflammatory, and autophagy-enhancing pathways. However, findings are preclinical and based on a single high dose administered immediately post-ischemia, which may not mirror real-world supplement use. For cardiovascular support, users should note that lumbrokinase’s benefits here were tied to early intervention in a controlled injury model, not chronic supplementation. Human trials are needed to validate these mechanisms and determine relevance to conditions like angina or post-cardiac surgery recovery. The study also underscores the importance of timing and Sirt1 activation, which could inform future therapeutic strategies but requires cautious interpretation for over-the-counter use.

Note: The study did not report baseline demographics (e.g., age, weight) for all rats, and no female animals were included, limiting sex-based conclusions.