To study the regulatory effect of tripterygium glycosides（TG）on ferroptosis of osteosarcoma cells via transcription factor EB（TFEB）-lysosome pathway.

Osteosarcoma U2OS cells were cultured and divided into control group, TG groups with different concentrations（10, 20, 40, 80, 160, 320 μmol/L）, negative control（NC）group（transfected with NC siRNA）, and NC + TG group（transfected with NC siRNA combined with 160 μmol/L TG）, si-TFEB + TG（transfected with TFEB siRNA combined with 160 μmol/L TG）. Cell proliferation activity was detected by CCK-8 assay, lysosome probe Lyso-Tracker activity was detected by flow cytometry, Fe²⁺ and reactive oxygen species（ROS）levels were detected by enzymolysis assay. Western blot analysis was performed to detect the expression levels of TFEB in total protein and nuclear protein and the expression levels of lysosome related proteins（LAMP1, LAMP2, CTSB, CTSD）and ferroptosis related proteins（GPX4, SLC7A11）in total protein.

The survival rate of TG groups with different concentrations was lower than that of the control group（P<0.05）, and the higher the concentration of TG, the lower the survival rate. The LysoTracker activity and the expression levels of LAMP1, LAMP2, GPX4 and SLC7A11 in total protein of low, medium and high concentration TG groups（40, 80, 160 μmol/L） were lower than those in the control group, the expression levels of Fe²⁺, ROS and TFEB in nuclear protein, the expressions of CTSB and CTSD in total protein were higher than those in the control group（P<0.05）. The survival rate, LysoTracker activity and the expression levels of LAMP1, LAMP2, GPX4 and SLC7A11 in total protein of si-TFEB + TG group were higher than those in the NC + TG group, the expression levels of Fe²⁺, ROS and TFEB in nuclear protein, the expression of CTSB and CTSD in total protein were lower than those in the NC + TG group（P<0.05）.

TG affects lysosomal function by promating TFEB nuclear translocation, and then promotes ferroptosis in osteosarcoma cells.

To study the clinical study of Biejiajian Pills（鳖甲煎丸）treating hepatitis B liver fibrosis（blood stasis in liver and spleen syndrome）.

A total of 102 patients with hepatitis B liver fibrosis（blood stasis in liver and spleen syndrome）admitted to the hospital from November 2022 to July 2024 were selected as the study objects and the patients were divided into two groups by random number table method. Fifty-one patients receiving conventional Western medicine were established as the control group and fifty-one patients receiving Biejiajian Pills on the basis of the conventional Western medicine were established as the experimental group. After treatment, the clinical effects of the two groups were observed and compared, including TCMsyndrome scores, hepatitis B virus e antigen（HBeAg）negative conversion rate, hepatitis B virus e antibody（HBe-Ab）positive conversion rate, liver function, liver fiber and inflammatory indicators before and after treatment.

After treatment, the TCMsyndrome scores of both groups decreased, and the scores of the experimental group decreased more significantly than that of the control group（P<0.05）. Compared with those in the control group, the levels of glutalanine transferase（ALT）, glutamic oxalate transferase（AST）and total bilirubin（TBIL）in the experimental group were lower, and the proportion of white ball（A/G）was higher（P<0.05）. Compared with those in the control group, the levels of laminin（LN）, hyaluronic acid（HA）, type Ⅲ procollagen（PC-Ⅲ）and type Ⅳ collagen（C-Ⅳ）in the experimental group were lower（P<0.05）. The conversion rate of HBeAg to negative was 49.02%（25/51）, and the conversion rate of HBeAb to positive was 41.18%（21/51）in the experimental group, which were higher than 27.45%（14/51）and 19.61%（10/51）in the control group（P<0.05）. Compared with those in the control group, the levels of interleukin-15（IL-15）, interleukin-16（IL-16）and transforming growth factor-β1（TGF-β1）in the experimental group were lower（P<0.05）.

Biejiajian Pills can effectively improve the liver function and liver fiber index, reduce the clinical symptoms and control the condition of patients with hepatitis B liver fibrosis（blood stasis in liver and spleen syndrome）, and has high clinical application value.

To observe the effect of Bushen Huoxue Formula（补肾活血方）on myocardial fibrosis and TGF-β1/Smads signaling pathway in rats with heart failure after myocardial infarction.

120 male SD rats aged 12 weeks were purchased and 20 were selected as the sham surgery group using the random number method. The remaining 100 rats underwent anterior descending coronary artery ligation, combined with starvation and exhaustive swimming to create a heart failure model after myocardial infarction. A total of 80 model rats were randomly divided into a model group, a Western medicine group, a Chinese medicine high dose group, a Chinese medicine medium dose group and a Chinese medicine low dose group. The rats in the Chinese medicine high, medium and low dose groups were given Bushen Huoxue Formula by gavage at a concentration ratio of 4∶2∶1. The western medicine group was given a suspension of sacubitril and valsartan sodium tablets by gavage. The model group and sham surgery group were given an equal amount of distilled water by gavage. After 4 weeks of continuous medication, ultrasound was used to detect the left ventricular end systolic diameter（LVESD）, left ventricular end diastolic diameter（LVEDD）, left ventricular ejection fraction（EF）and left ventricular short axis shortening rate（FS）in six groups. Masson staining was used to observe the degree of myocardial fibrosis in the six groups and the collagen volume fraction（CVF）was measured. Western blotting（WB）was used to measure the protein expression levels of TGF-β1, p-Smad2, p-Smad3, Collagen Ⅰ and Collagen Ⅲ in the myocardial tissue of the six groups. Fluorescence quantitative polymerase chain reaction（PCR）was used to detect the mRNA expressions of Smad6 and Smad7 in the myocardial tissue of the six groups.

After 4 weeks of medication, compared with those of the sham surgery group, the levels of LVESD and LVEDD of the model group increased, while the levels of EF and FS decreased. The myocardial structure was disordered, CVF increased, and the protein expressions of TGF-β1, p-Smad2, p-Smad3, Collagen Ⅰ and Collagen Ⅲ in myocardial tissue increased. The mRNA expressions of Smad6 and Smad7 decreased（P<0.01）. Compared with those of the model group, the levels of LVESD and LVEDD of rats in the western medicine group and the Chinese medicine low, medium and high dose groups were reduced, while the levels of EF and FS were increased. The myocardial structure was neat, CVF was reduced, and the protein expressions of TGF-β1, p-Smad2, p-Smad3, Collagen Ⅰ and Collagen Ⅲ in myocardial tissue was reduced. The expressions of Smad6 mRNA and Smad7 mRNA were increased（P<0.05 or P<0.01）. Compared with the Chinese medicine high dose group, the Chinese medicine medium dose group showed an increase in the levels of LVESD and LVEDD, a decrease in the levels of EF and FS, an increase in the protein expressions of TGF-β1, p-Smad2, p-Smad3, Collagen Ⅰ and Collagen Ⅲ in myocardial tissue, and a decrease in mRNA expressions of Smad6 and Smad7（P<0.01）. Compared with the Chinese medicine medium dose group, the Chinese medicine low dose group showed an increase in the levels of LVESD and LVEDD, a decrease in the levels of EF and FS, an increase in the protein expressions of TGF-β1, p-Smad2, p-Smad3, Collagen Ⅰ and Collagen Ⅲ in myocardial tissue, and a decrease in mRNA expressions of Smad6 and Smad7（P<0.01 or P<0.05）.

Bushen Huoxue Formula can improve myocardial fibrosis in rats with heart failure after myocardial infarction, and its mechanism of action may be related to the inhibition of TGF-β1/Smads activation by Bushen Huoxue Formula.

To observe the anti-inflammatory effect of Fuyanshu Capsule（妇炎舒胶囊, FYS）on sequelae of pelvic inflammatory disease（SPID）model rats on Krüppel-like factor 4（KLF4）, Toll-like receptor 2（TLR2）, nuclear factor-kappa B（NF-κB）and myeloid differentiation factor 88（MyD88）.

Thirty-six rats were randomly divided into blank group, model group, Kangfuyan Capsule（康妇炎胶囊）group（KFY group）, FYS high-dose group, FYS medium-dose group, FYS low-dose group. The SPID animal model was established by the method of mixed bacterial liquid injection and mechanical injury. The blank group was treated with distilled water by gavage, and the other groups were given the corresponding drug suspension by gavage for 21 days. HE staining was used to observe the morphology of uterine tissue and score the pathological sections. The mRNA expressions of TLR2, MyD88 and KLF4 were determined by RT-PCR, the expression of NF-κB was observed by immunohistochemistry method, and the relative protein expressions of TLR2, MyD88 and KLF4 in uterine tissues of each group were determined by Western Blot. The correlation between KLF4 and key factors of TLR2/MyD88/NF-κB pathway was analyzed.

Compared with those in the model group, the scores of uterine tissue inflammation in KFY group, FYS medium - and high-dose groups were significantly decreased（P<0.05）. KLF4 protein in KFY group and FYS high-dose group was significantly increased（P<0.01）. The protein and mRNA of TLR2 in KFY group and FYS high-dose group were significantly decreased（P<0.05）. MyD88 protein in KFY group, FYS high-and medium-dose groups was significantly decreased（P<0.05）, and MyD88 mRNA in KFY group and FYS high-dose group was significantly decreased（P<0.05）. The expressions of NF-κB protein in KFY group, FYS medium - and high-dose groups were significantly decreased（P<0.05）. The expression of KLF4 protein was negatively correlated with the expressions of TLR2 protein, MyD88 protein and NF-κB protein（P<0.05）.

FYS can inhibit the TLR2/MyD88/NF-κB pathway by up-regulating KLF4 expression.

To investigate the mechanism of action of Bufei Decoction（补肺汤）in intervening chronic obstructive pulmonary disease（COPD）lung Qi deficiency by modulating the levels of mitochondrial autophagy mediated by phosphatase and tensin homolog-induced putative kinase protein 1（PINK1）/RBR domain E3 ubiquitin protein ligase（Parkin）signaling path-way.

The rats were randomly divided into the control group and the modeling group, and a rat model of COPD lung Qi deficiency was created by using passive smoke inhalation combined with intra-airway lipopolysaccharide drip. At the end of modeling, the rats in the modeling group were randomly divided into the model group, Bufei Decoction medium-dose group, Bufei Decoction high-dose group and 3-methyladenine（3-MA）group. The Bufei Decoction medium - and high-dose groups were given Bufei Decoction drug solution by gavage（7.29, 14.58 g·kg^-1）, and 3-MA group was given 3-MA（15 mg·kg^-1）by intraperitoneal injection, and each group was intervened with the drug once daily for 28 d consecutively. Hematoxylineosin（HE）staining was used to observe the pathological changes in lung tissues. The transmission electron microscopy was used to observe ultrastructural changes in alveolar type Ⅱ epithelial cells in lung tissues. The immunohistochemistry（IHC）method was used to detect the positive expressions of PINK1, Parkin, autophagy receptor protein P62（sequestosome 1, P62/SQSTM1）and microtubule-associated protein 1 light chain 3（LC3）proteins in lung tissues and protein immunoblotting（Western blot）to detect the expressions of PINK1 in mitochondria in lung tissues, Parkin, P62, LC3Ⅱ/LC3I protein expression in mitochondria of lung tissues. Flow cytometry detected the changes of mitochondrial membrane potential in lung tissues. The reactive oxygen species fluorescent probe dichloro-dihydro-fluorescein diacetate（DCFH-DA）and mitochondrial superoxide（MitoSOX）red fluorescent probe were used to determine the levels of reactive oxygen species（ROS）and mitochondrial reactive oxygen species（mtROS）in lung tissues by flow cytometry, respectively. Western blot detected the expressions of nuclear factor-κB P65（NF-κB P65）and phosphorylation of nuclear factor-κB P65（p-NF-κB P65）proteins in lung tissues.

Compared with that in the control group, the lung tissue damage in the model group was severe. Compared with that in the model group, the pathological damages in the Bufei Decoction medium - and high-dose groups and 3-MA group were improved to different degrees. Compared with those of the control group, the lung tissue of the model group showed severe damage to alveolar type Ⅱ epithelial cells and their mitochondrial structure, with a decrease in mitochondria and an increase in autophagic vesicles. Compared with those of the model group, the alveolar type Ⅱ epithelial cells and their mitochondrial structure of the model group showed a lesser degree of damage in the Bufei Decoction medium - and high-dose groups and the 3-MA group, with a relatively higher increase in mitochondria and a decrease in autophagic vesicles. Compared with those in the control group, the protein expressions of PINK1, Parkin, LC3 and LC3Ⅱ/LC3I were up-regulated（P<0.01）and the protein expression of P62 was down-regulated（P<0.01）in the lung tissues and mitochondria of lung tissue in the model group. Compared with those in the model group, the protein expressions of PINK1, Parkin and LC3Ⅱ/LC3I were up-regulated（P<0.01）and the protein expression of P62 was down-regulated（P<0.01）in the lung tissues and mitochondria of lung tissue in the Bufei Decoction medium - and high-dose groups and 3-MA group. The protein expressions of PINK1, Parkin, LC3 and LC3Ⅱ/LC3I were down-regulated（P<0.05, P<0.01）and P62 protein expression was up-regulated（P<0.01）. Compared with those in the control group, the mitochondrial membrane potential of lung tissues in the model group was decreased（P<0.01）, the levels of ROS and mtROS were up-regulated（P<0.01）, the difference in the expression of NF-κB P65 protein was not statistically significant, and the expression of p-NF-κB P65 protein was up-regulated（P<0.01）. Compared with those of the model group, the mitochondrial membrane potential in the lung tissues of the Bufei Decoction medium - and high-dose groups and the 3-MA group were elevated（P<0.01）, the levels of ROS and mtROS were down-regulated（P<0.01）, and the differences in the expression of NF-κB P65 proteins were not statistically significant, and the expression of p-NF-κB P65 protein was down-regulated（P<0.01）.

Bufei Decoction inhibited lung tissue ROS levels and the activation of NF-κB P65, thereby attenuating the oxidative damage and inflammatory responses in the lung of COPD lung Qi deficiency, and its mechanism of action may be related to the inhibition of the level of mitochondrial autophagy mediated by the PINK1/Parkin signaling pathway.

To explore the effects of Danggui Buxue Decoction（当归补血汤）combined with acupuncture on the levels of blood homocysteine（Hcy）, nerve growth factor（NGF）, insulin-like growth factor-1（IGF-1）and vascular endothelial growth factor（VEGF）and the changes in nerve conduction function in diabetic patients with peripheral neuropathy.

This paper collected 120 diabetic patients with peripheral neuropathy admitted to the hospital between January 2022 and January 2024, and were randomly divided into test group and control group. The control group used conventional Western medicine treatment, and the test group used acupuncture and Danggui Buxue Decoction. TCMsyndrome scores, diabetic peripheral neuropathy scores, diabetic neuropathy score（DNS）, clinical efficacy, serum levels of Hcy, NGF, IGF-1 and VEGF and nerve conduction function were compared.

There was no significant difference in TCMsyndrome scores, DNS, the serum levels of Hcy, NGF, IGF-1 or VEGF, the conduction velocities of median nerve motor conduction（MCV）and tibial nerve sensory conduction（SCV）between the two groups before treatment（P>0.05）. The scores of TCMsyndromes and DNS in both groups were significantly lower after treatment and the scores and DNS in the test group were significantly lower than those in the control group（P<0.05）. The clinical effective rate in the test group was significantly higher than that in the control group（P<0.05）. After treatment, the serum levels of Hcy and VEGF in the two groups were significantly lower than those before treatment, the serum levels of NGF and IGF-1, conduction velocities of MCV and SCV on both sides were significantly higher than those before treatment, and the decrease/increase amplitude in the test group was significantly higher than that in the control group（P<0.05）.

- Acupuncture and Danggui Buxue Decoction have obvious effect and can effectively improve the serum levels of Hcy, NGF, IGF-1 and VEGF and the nerve conduction function of the diabetic patients with peripheral neuropathy.

To investigate the effect of Guben Qingyuan Prescription（固本清源方）on inhibiting cancer-associated fibroblast（CAF） in the development of resistance to enzalutamide.

A tumor-bearing mouse model of enzalutamide-resistant prostate cancer cells was established to observe the effects of Guben Qingyuan Prescription combined with enzalutamide on tumor growth and CAF in tumor tissues. The effects of Guben Qingyuan Prescription on CAF transformation were assessed using immunofluorescence. CAF proliferation was evaluated by the CCK8 assay, and the influence of Guben Qingyuan Prescription on CAF-derived factors was measured via enzyme-linked immunosorbent assay（ELISA）.

The tumor inhibition rate of the Guben Qingyuan Prescription combined with enzalutamide ranged from 29% to 47%. In the medium - and high-dose groups, the combination treatment showed a statistically significant difference compared to the enzalutamide-only group（P<0.01）. Immunofluorescence and immunohistochemistry results demonstrated that the expressions of CAF markers fibroblast activation protein-α（FAP）and α-smooth muscle actin（α-SMA）in tumor tissues of enzalutamide-resistant mice were significantly higher than those in the group inoculated with prostate cancer C4-2B cells. The medium - and high-dose Guben Qingyuan Prescription combined with enzalutamide groups significantly inhibited the expressions of FAP and α-SMA compared to the enzalutamide-only group（P<0.05）. Additionally, immunofluorescence showed that serum containing medium - and high-dose Guben Qingyuan Prescription groups could inhibit the expressions of FAP and α-SMA in vitro. After 48 and 72 hours of treatment, the inhibition rates of the medium - and high-dose Guben Qingyuan Prescription groups significantly increased, with a statistically significant difference compared to the control group（P<0.05）. Further studies revealed that Guben Qingyuan Prescription reduced the concentrations of transforming growth factor-β1（TGF-β1）, tumor necrosis factor-α（TNF-α）, stromal cell-derived factor-1（SDF-1）, Wingless/Integrated-3a（Wnt3a）and matrix metalloproteinase 2（MMP2）in CAF supernatants.

Guben Qingyuan Prescription has a significant effect in delaying resistance to enzalutamide, a novel endocrine therapy for prostate cancer, and its mechanism of action may be related to the inhibition of CAF.

The aim of this study was to investigate the effects of myristicin on the regulation of endonuclease/exonuclease/phosphatase family domain containing 1（EEPD1）expression and its subsequent impact on the proliferation, migration, invasion and apoptosis of pulmonary squamous cell carcinoma.

Molecular docking techniques were employed to analyze the interaction between myristicin and the target protein EEPD1. Immunohistochemistry method was used to assess the levels of EEPD1 protein in lung squamous carcinoma and adjacent paracancerous tissues on tissue chips. The gene expression activity in cell lines was evaluated using real-time quantitative polymerase chain reaction（qRT-PCR）, while the effect of myristicin on the proliferation of lung squamous carcinoma cells KNS-62 and NCI-H226 was assessed with Cell Counting Kit-8（CCK-8）. Scratch assay and Transwell migration and invasion experiments were conducted to examine the impact of myristicin on the migration and invasion capabilities of lung squamous carcinoma cells. Flow cytometry method was utilized to determine the influence of myristicin on the apoptosis of lung squamous carcinoma cells, and Western blot（WB）was employed to analyze the expression of EEPD1 protein in these cells.

Myristicin could form specific binding with the EEPD1 protein. Higher EEPD1 positive signal intensity was observed in lung squamous carcinoma tissue samples compared to adjacent paracancerous tissue control areas. CCK-8 assay results demonstrated that myristicin significantly inhibited the proliferation of lung squamous carcinoma cells. A slower scratch healing rate suggested that myristicin could inhibit the migration of lung squamous carcinoma cells. Transwell assay results similarly showed that myristicin could inhibit the migration and invasion of lung squamous carcinoma cells. Flow cytometry data revealed that myristicin promoted the apoptosis of lung squamous carcinoma cells, while WB analysis indicated that myristicin reduced the expression level of EEPD1 protein.

In vitro experimental evidence supports that myristicin exerts its anticancer effects by down-regulating the expression of EEPD1 protein, specifically manifested in inhibiting the proliferation, migration and invasion of pulmonary squamous cell carcinoma and promoting cell apoptosis.

This study explored the pharmacological effect and mechanism of wogonin on lung metastasis of breast cancer after myocardial infarction, and provided potential drugs and experimental basis for the treatment of lung metastasis of breast cancer.

In the experiment, the mouse model of myocardial infarction and breast cancer was established by 6-7 weeks old female balb/c mice, and the effect of wogonin on lung metastasis of breast cancer after myocardial infarction and macrophages in mouse tumors was detected. THP-1, RAW264.7 and bone marrow-derived macrophages（BMDM）cells were induced in vitro to construct macrophage polarization model, and the effect of wogonin on macrophage polarization and the changes of key proteins regulating polarization were detected.

The results showed that compared with those of the model group, the number of lung tumor metastasis, the weight of breast tumor, cardiac function and cardiac inflammation were significantly reduced, and the expression of M2 macrophages in tumor was significantly reduced in the wogonin group. In vitro experiments showed that wogonin significantly inhibited the M2 polarization of macrophages, reduced the phosphorylation of signal transducer and activator of transcription 6（STAT6）and inhibited the migration of MDA-MB 231 cells.

The above results indicate that wogonin can inhibit the lung metastasis of breast adenocarcinoma after myocardial infarction, and its mechanism may be realized by inhibiting the phosphorylation of STAT6 and then affecting the M2 polarization of macrophages in the tumor.