The anti-HIV activities of a pine cone extract (YNS-PY-F) from Pinus yunnanensis have been evaluated, and its mechanisms of action were also explored. The pine cone extract, YNS-PY-F, potently inhibited HIV-1_IIIB, HIV-1_RF, HIV-1_A17, HIV-1_AO18 and HIV-2_ROD and induced cytopathic effect in C8166 cells with EC₅₀ values of 0.96 μg/mL, 1.53 μg/mL, 0.88 μg/mL, 7.20 μg/mL and 6.17 μg/mL, respectively. The quantification of a p24 production assay showed that YNS-PY-F significantly inhibited the acute replication of HIV-1_IIIB, HIV-1_RF, HIV-1_A17 and HIV-1_AO18 in C8166 cells. An MTT assay showed that YNS-PY-F also significantly inhibited the HIV-1_IIIB induced cytolysis in MT-4 cells with an EC₅₀ value of 2.22 μg/mL. The mechanism assays showed that YNS-PY-F had potent inhibitory effects on the fusion between infected cells and uninfected cells, and the activity of HIV-1 reverse transcriptase, with EC₅₀ values of 7.60 μg/mL and 4.60 μg/mL, respectively. Overall, these data suggest that the pine cone extract from Pinus yunnanensis has potent inhibitory activities against HIV-1_IIIB, HIV-1_RF, RT inhibitor-resistant strains HIV-1_A17 and HIV-1_AO18, and HIV-2_ROD, and its anti-HIV mechanisms include inhibition of HIV entry and inhibition of reverse transcriptase activity.

Lung cancer remains the leading cause of cancer-related mortality worldwide. Tumor-associated macrophages (TAMs) and epithelial-mesenchymal transition (EMT) are key drivers of lung cancer metastasis and drug resistance. M2-polarized TAMs dominate the immunosuppressive tumor microenvironment (TME) and promote EMT through cytokines such as TGF-β, IL-6, and CCL2. Conversely, EMT-transformed tumor cells reinforce TAM recruitment and M2 polarization through immunomodulatory factors such as CCL2 and ZEB1, thereby establishing a bidirectional interplay that fuels tumor progression. Current evidence on this interaction remains fragmented, and a comprehensive review of the TAM-EMT regulatory network and its therapeutic implications is lacking. This review systematically integrates the bidirectional regulatory mechanisms between TAMs and EMT, highlighting their roles in lung cancer progression. It also summarizes emerging therapeutic strategies targeting TAM polarization and the EMT process, emphasizing their potential for clinical translation. This study fills the gap in systematic reviews on the interaction between TAMs and EMT, providing a comprehensive theoretical foundation for future research and the development of novel lung cancer therapies.

Pulmonary fibrosis (PF) is an interstitial lung disease characterized by inflammation and fibrotic changes, with an unknown cause. In the early stages of PF, severe inflammation leads to the destruction of lung tissue, followed by upregulation of fibrotic factors like Transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF), which disrupt normal tissue repair. Geniposide, a natural iridoid glycoside primarily derived from the fruits of Gardenia jasminoides Ellis, possesses various pharmacological activities, including liver protection, choleretic effects, and anti-inflammatory properties. In this study, we investigated the effects of Geniposide on chronic inflammation and fibrosis induced by bleomycin (BLM) in mice with pulmonary fibrosis (PF). PF was induced by intratracheal instillation of bleomycin, and Geniposide(100/50/25mg•kg^-1) was orally administered to the mice once a day until euthanasia(14 day/28 day). The Raw264.7 cell inflammation induced by LPS was used to evaluate the effect of Geniposide on the activation of macrophage. Our results demonstrated that Geniposide reduced lung coefficients, decreased the content of Hydroxyproline, and improved pathological changes in lung tissue. It also reduced the number of inflammatory cells and levels of pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) of bleomycin-induced PF mice. At the molecular level, Geniposide significantly down-regulated the expression of TGF-β1, Smad2/3, p38, and CTGF in lung tissues of PF mice induced by bleomycin. Molecular docking results revealed that Geniposide exhibited good binding activity with TGF-β1, Smad2, Smad3, and p38. In vitro study showed Geniposide directly inhibited the activation of macrophage induced by LPS. In conclusion, our findings suggest that Geniposide can ameliorate bleomycin-induced pulmonary fibrosis in mice by inhibiting the TGF-β/Smad and p38MAPK signaling pathways.