Rehmannia for Heart Health? What the Science Says

Key Findings

The study demonstrated that TMYX, a traditional Chinese medicine containing Rehmannia glutinosa, significantly reduced coronary heart disease (CHD) risk factors in patients, including lowering apolipoprotein B (ApoB), endothelin 1 (ET-1), nuclear factor κB (NF-κB), and homocysteine (Hcy) levels, while increasing the anti-inflammatory apolipoprotein A/ApoB ratio. In vitro, an ethanol extract of TMYX (EETMYX) suppressed foam cell formation and inflammation in RAW264.7 macrophages by upregulating estrogen receptor 1 (ESR1) and inhibiting NF-κB signaling pathway activation. These findings align with bioinformatics predictions, suggesting TMYX’s anti-inflammatory effects are mediated through ESR1 and NF-κB regulation.

Study Design

This 2021 study combined clinical trial data, microarray analysis, and in vitro experiments. The clinical trial included 8 CHD patients who received TMYX orally for 8 weeks. Microarray and Ingenuity Pathway Analysis (IPA) assessed transcriptional changes in patient samples. In vitro, RAW264.7 macrophages were induced with oxidized low-density lipoprotein (ox-LDL) to model CHD inflammation, followed by EETMYX treatment (25–100 μg/mL). No control group or randomization details were provided for the clinical trial, and demographics (e.g., age, gender) were unspecified.

Dosage & Administration

Patients received 40 pills of TMYX twice daily for 8 weeks. The in vitro experiments used EETMYX at concentrations of 25–100 μg/mL. The study did not specify pill composition ratios or administration timing relative to meals.

Results & Efficacy

• Clinical Trial: TMYX reduced ApoB (p < 0.05), ET-1 (p < 0.05), NF-κB (p < 0.01), and Hcy (p < 0.05), while increasing ApoA/ApoB ratio (p < 0.05).
• In Vitro: EETMYX (100 μg/mL) suppressed lipid deposition by 60% and reduced pro-inflammatory cytokines (MCP-1, TNF-α, IL-6) by 40–70% (p < 0.01 for all). EETMYX also blocked NF-κB pathway activation by preventing IκBα degradation and IKKα/β phosphorylation.
• Bioinformatics: IPA linked TMYX-induced gene expression changes to inflammation-related pathways, corroborating in vitro results.

Limitations

1. Small sample size (n=8) in the clinical trial limits statistical power and generalizability.
2. Lack of controls: No placebo or comparator group in the clinical trial; in vitro experiments lacked validation in human cells or animal models.
3. Short duration (8 weeks) may not capture long-term efficacy or safety.
4. Unspecified demographics: Age, gender, or comorbidities of patients were not reported.
5. Combination therapy confounding: TMYX contains 11 herbs, so Rehmannia’s individual contribution remains unclear.
6. In vitro limitations: Murine macrophages may not fully mirror human inflammatory responses.

Clinical Relevance

TMYX shows potential as an adjunct therapy for CHD by improving biochemical markers of inflammation and lipid metabolism. However, the absence of placebo-controlled trials and the small sample size prevent definitive conclusions. Patients should not replace standard CHD treatments (e.g., statins, anticoagulants) with TMYX or Rehmannia-based supplements without medical supervision. Future studies should isolate Rehmannia’s active compounds and test TMYX in larger, randomized trials to confirm its role in modulating ESR1 and NF-κB pathways. For supplement users, this research highlights the need for caution in interpreting results from multi-herb formulations and underscores the importance of mechanistic clarity before clinical adoption.

Study URL: https://pubmed.ncbi.nlm.nih.gov/33838287/