Related Experiment Video
Updated: Apr 23, 2026
Establishment of Hepatocarcinoma in BALB/c-nu Mice and Investigation of the Therapeutic Effect of the Sanleng Jiashen Formula
Published on: January 26, 2024
[Effect of bear bile powder on STAT3 pathway in hepatocellular carcinoma xenograft]
Objective:
To observe the effect of bear bile powder (BBP) on the STAT3 pathway and its downstream target genes of nude mice hepatocellular carcinoma (HCC) xenograft, and to explore its mechanism for treating HCC.
Methods:
The subcutaneous xenograft model was established using HepG2 cells. When the subcutaneous transplanted tumor was formed, naked mice were randomly divided into two groups, the BBP group and the control group. Mice in the BBP group were administered with BBP by gastrogavage, once daily for 3 consecutive weeks, while mice in the control group were administered with normal saline by gastrogavage, once daily for 3 consecutive weeks. The body weight and the tumor volume were measured once per week. By the end of medication, the tumor weight was weighed and the tumor inhibition ratio calculated. The apoptosis of the tumor tissue was detected by TdT-mediated dUTP nick end labeling (TUNEL). The expression of Bcl2-associated X protein (Bax), B cell lymphoma/eukemina-2 (Bcl-2), cyclin-dependent protein kinase (CDK4), cyclinD1 were detected by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression levels of signal transducers and transcription activators 3 (p-STAT3), proliferating cell nuclear antigen (PCNA), Bax, Bcl-2, CDK4, and cyclinD1 were determined by immunohistochemistry.
Results:
BBP could inhibit the tumor volume and tumor weight, showing statistical difference when compared with the control group (P < 0.01). Results of TUNEL showed that BBP could significantly induce the apoptosis of hepatoma carcinoma cells. Results of RT-PCR showed that BBP could up-regulate the expression of Bax and down-regulate mRNA expression of Bcl-2, CDK4, and cyclinD1. Immunohistochemical results showed that BBP could up-regulate the expression of Bax and inhibit the protein expression of p-STAT3, PCNA, Bcl-2, CDK4, and cyclinD1.
Conclusion:
BBP could induce the apoptosis of hepatoma carcinoma cells and inhibit their proliferation by regulating STAT3 pathway.
Insights
Bear bile powder (BBP) effectively inhibits hepatocellular carcinoma (HCC) growth in nude mice by inducing cancer cell apoptosis and reducing proliferation. This study reveals BBP
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Context:
- Hepatocellular carcinoma (HCC) is a significant global health concern with limited effective treatments.
- Bear bile powder (BBP) has a long history of use in traditional medicine, but its therapeutic mechanisms in HCC require scientific validation.
- The STAT3 signaling pathway plays a crucial role in HCC development and progression.
Purpose:
- To investigate the anti-cancer effects of BBP on HCC xenografts in nude mice.
- To elucidate the molecular mechanisms underlying BBP's action, focusing on the STAT3 pathway and its downstream targets.
- To evaluate BBP's impact on tumor growth, apoptosis, and proliferation markers.
Summary:
- Bear bile powder (BBP) administration significantly reduced tumor volume and weight in a nude mouse model of hepatocellular carcinoma (HCC).
- BBP treatment led to increased apoptosis and decreased proliferation in tumor tissues, as evidenced by TUNEL and immunohistochemical analyses.
- Molecular analysis revealed that BBP modulates the STAT3 pathway, upregulating Bax and downregulating Bcl-2, CDK4, and cyclinD1 expression.
Impact:
- This research provides scientific evidence for the efficacy of BBP in HCC treatment.
- Understanding BBP's mechanism via STAT3 pathway regulation could lead to novel therapeutic strategies for HCC.
- The findings support further investigation into BBP as a potential adjuvant or alternative therapy for liver cancer.
