Unlike the traditional staging treatment of tumors, the core of “Green Tumor Treatment” is to divide the treatment of tumors into three stages: Hegemony (directly targeting the cancer focus), Kingship (supporting the body’s vital energy and eliminating pathogenic factors), and Imperialism (improving the internal environment), based on the urgency of the tumor and the patient’s physical condition. This approach guides the clinical treatment of tumors. Its treatment system incorporates all minimally invasive and low-damage treatment methods, combining internal and external treatments, traditional Chinese medicine and Western medicine, as well as local and systemic treatments. It aims to maximize treatment outcomes while ensuring the patient’s quality of life, which is highly consistent with the treatment goals for primary liver cancer. This review aims to explore the integrated Traditional Chinese and Western medicine treatment model for primary liver cancer under the guidance of the Green Tumor Treatment concept.

PVT is a harmful event in cirrhosis, and the prevention and treatment of PVT are important in the management of cirrhosis and portal hypertension. The study aimed to observe the efficacy of Danggui Buxue Decoction (DBD) on portal vein thrombosis (PVT) in cirrhosis and to elucidate the related mechanism using a modified animal model.

A model of PVT in cirrhosis was established by partial portal vein ligation and intraperitoneal injection of CCl4 in rats, which showed obvious PVT with intra- and extravenous thrombosis as well as liver cirrhosis. Rats were randomly assigned into four groups and received intragastric administration of DBD (12 g/kg/day) or rivaroxaban (20 mg/kg/day) for 6 weeks.

DBD attenuated collagen deposition and reduced thrombus formation in model livers, increased portal vein blood flow, expanded the portal vein diameter, and reduced prothrombin time and international normalized ratio in the model rats. In addition, DBD reduced hepatic von Willebrand factor and plasminogen activator inhibitor-1 expression and increased hepatic fibrin degradation product content in the liver tissues of model rats.

We modified a model of cirrhotic PVT in rats and found that DBD had a good effect on PVT and liver fibrosis, with the mechanisms related to the enhancement of portal vein blood flow and the protection against endothelial cell injury.

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and mortality rates worldwide, in which immune evasion mechanisms play a crucial role in its progression and treatment. Natural killer group 2D ligands (NKG2DL), as key molecules activating immune cells, significantly influence the immune evasion of liver cancer through their regulatory mechanisms. This review summarizes the regulatory mechanisms of NKG2DL expression, including genetic, signaling pathway, non-coding RNA, and stress response modulation, and discusses their expression patterns and clinical relevance in HCC. Studies have shown that the expression status of NKG2DL not only impacts patient prognosis and therapeutic response but also provides potential targets for HCC immunotherapy. Future research should focus on the molecular networks regulating their expression and their synergy with immunotherapy to provide a theoretical basis for developing more precise diagnostic and personalized treatment strategies for HCC.

PVT is a harmful event in cirrhosis, and the prevention and treatment of PVT are important in the management of cirrhosis and portal hypertension. The study aimed to observe the efficacy of Danggui Buxue Decoction (DBD) on portal vein thrombosis (PVT) in cirrhosis and to elucidate the related mechanism using a modified animal model.

A model of PVT in cirrhosis was established by partial portal vein ligation and intraperitoneal injection of CCl4 in rats, which showed obvious PVT with intra- and extravenous thrombosis as well as liver cirrhosis. Rats were randomly assigned into four groups and received intragastric administration of DBD (12 g/kg/day) or rivaroxaban (20 mg/kg/day) for 6 weeks.

DBD attenuated collagen deposition and reduced thrombus formation in model livers, increased portal vein blood flow, expanded the portal vein diameter, and reduced prothrombin time and international normalized ratio in the model rats. In addition, DBD reduced hepatic von Willebrand factor and plasminogen activator inhibitor-1 expression and increased hepatic fibrin degradation product content in the liver tissues of model rats.

We modified a model of cirrhotic PVT in rats and found that DBD had a good effect on PVT and liver fibrosis, with the mechanisms related to the enhancement of portal vein blood flow and the protection against endothelial cell injury.

To investigate the mechanism underlying the role of the Nrf2-Keap1-Are oxidative stress pathway in liver fibrosis related to qi deficiency and blood stasis.

A total of 30 Sprague–Dawley rats were randomly divided into a normal group, a qi deficiency and blood stasis group, and a Fuzheng Huayu treatment group. After death, body weights and liver wet weights were measured and liver sections were stained with Sirius red. RT-PCR was used to detect the mRNA expression levels of α-SMA, Nrf2, Keap1, and β-actin, and western blotting was used to detect the protein expression levels of α-SMA, LC3II, P62, and LC3II.

The Ishak score for liver fibrosis in the qi deficiency and blood stasis group was higher than that in the liver fibrosis group (P < 0.05) and decreased significantly following Fuzheng Huayu therapy (P < 0.05). As determined by PCR, α-SMA mRNA levels were highest in the qi deficiency and blood stasis group and were significantly higher than those in the treatment group (P < 0.05). Nrf2 and Keap1 mRNA expression levels were lowest in the qi deficiency and blood stasis group but increased significantly after treatment (P < 0.05). Western blotting showed that α-SMA and LC3II levels were highest in the qi deficiency and blood stasis group (P < 0.05) and decreased significantly after treatment (P < 0.05). The expression levels of P62, Nrf2, and Nqo1 were lowest in the qi deficiency and blood stasis group and increased significantly after treatment (P < 0.05).

LC3II can down-regulate the expression of P62 in liver tissues of rats with qi deficiency and blood stasis, thereby inhibiting the activation of the Nrf2-Keap1-Are antioxidant stress pathway and aggravating liver fibrosis. However, this process can be reversed by strengthening qi and activating blood circulation to alleviate blood stasis.

To compare the clinical features of viral and cryptogenic liver cancer and to provide evidence of or reference the clinical identification of cryptogenic liver cancer and diagnosis and treatment using Chinese and Western medicine.

A retrospective analysis of the clinical data (general conditions, laboratory indicators, initial symptoms, and Traditional Chinese medicine (TCM) syndrome types) of 92 cases of viral liver cancer (VLC) and 36 cases of cryptogenic liver cancer (CLC) was performed by using SPSS version 20.0 statistical software.

There were significant differences in triglyceride, γ-glutamyl transpeptidase, and alkaline phosphatase levels, liver fibrosis index (Fibrosis 4 Score, APRI), and initial symptoms (P < 0.05) between VLC and CLC. However, there was no statistical difference in TCM syndrome types. Among the 128 patients with primary liver cancer, there was a high proportion of women with cryptogenic liver cancer. Compared to the VLC group, the CLC group was older, had a lower incidence of cirrhosis, and had a higher proportion of surgical resection.

Although the number of research cases was limited, the occurrence of cryptogenic liver cancer was more likely to be associated with abnormal metabolic factors. Cryptogenic liver cancer should be considered in the differential diagnosis when liver fibrosis indicators are detected.