ArticleEvidence-based complementary and alternative medicine : eCAM2022
Hugan Buzure Induces Autophagy and Apoptosis in Hepatocellular Carcinoma by Inhibiting PI3K/Akt/mTOR Signaling Pathway.
Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- To Prune or to Protect: Complement-Mediated Microglial Synaptic Pruning as a Therapeutic Target in Neuropathic Pain.Molecular neurobiology · 2026Review
- Stratified Efficacy and Peripheral Neuroinflammatory Mechanisms of Jin's Tongue Triple Acupuncture as Adjunctive Therapy for Subacute Post-Stroke Broca Aphasia: A 1:1 PSM Retrospective Cohort Study.Journal of molecular neuroscience : MN · 2026Article
- Targeting mTOR with curcumin: therapeutic implications for complex diseases.Inflammopharmacology · 2025Review
- Targeting the mTOR Pathway in Hepatocellular Carcinoma: The Therapeutic Potential of Natural Products.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study explored the effects of Hugan Buzure (HBR) on cell apoptosis and autophagy in hepatocellular carcinoma (HCC) and the molecular mechanisms of the PI3K/Akt/mTOR signaling pathway. HepG2 and Huh7 cell viability was detected by the tetramethylazolium salt colorimetric (MTT) method. Cell proliferation was measured using the colony formation method. Hoechst 33258 staining and flow cytometry were employed to detect apoptosis. In addition, immunofluorescence was carried out to evaluate the expression of LC3. Western blot was performed to detect the expression of Bcl-2, Bax, Caspase-3, LC3, Beclin1, p62 (SQSTM1), and PI3K/Akt/mTOR signal pathway-related proteins in HCC cells. This work verified that HBR reduced HepG2 and Huh7 cell proliferation in a concentration-dependent manner. Treatment with HBR caused an obvious improvement of the apoptosis rate, accompanied by the increase in Bax/Bcl2, Caspase3, LC3II, and Beclin1 levels, respectively. Furthermore, HBR downregulated the expression of p62, p-PI3K, p-Akt, and p-mTOR proteins. HBR combined with HCQ enhanced HBR-induced apoptosis. In conclusion, HBR induced autophagy and apoptosis through PI3K/Akt/mTOR signaling pathway, leading to HCC cell death. This research preliminarily suggested the potential role of HBR in the treatment of HCC.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.