Rheumatoid arthritis (RA) is a widespread autoimmune disease that significantly impacts the lives of RA patients. It is often typified as swelling and deformation of small joints, as well as systemic inflammation. Rhodiola rosea has been utilized for millennia to treat various ailments and is known to contain numerous active compounds, including saponins, volatile oils, coumarins, and flavonoids. Recent studies have underscored the pivotal role of salidroside (SAL), a key constituent of Rhodiola rosea L. Modern research indicates that SAL has various pharmacological activities, such as its antioxidant, anti-inflammatory, anti-fatigue, and anti-cancer effects. Despite this, the pathogenesis of RA remains highly complex, and a notable lack exists in overview studies investigating the anti-RA mechanisms of SAL. Therefore, the purpose of this article is to review the present research efforts on the anti-RA mechanisms of SAL and to explore future research prospects for this compound.

Sacha Inchi (Plukenetia volubilis L) (SI) is a traditional natural medicine from tropical rainforests of Amazon region in South America. As a raw material for edible oil, it has various pharmacological effects such as antioxidant, anti-inflammatory, hypolipidemia, and blood pressure lowering, which have attracted increasing attentions of pharmacists. This has prompted researchers to explore its pharmacological effects for potential applications in certain diseases. Among these, the study of its anti-inflammatory effects has become a particularly interesting topic, especially in rheumatoid arthritis (RA). RA is a systemic autoimmune disease, and often accompanied by chronic inflammatory reactions. Despite significant progress in its treatment, there is still an urgent need to find effective anti-RA drugs in regard to safety. This review summarizes the potential therapeutic effects of SI on RA by modulating gut microbiota, targeting inflammatory cells and pathways, and mimicking biologic antibody drugs, predicting the application prospects of SI in RA, and providing references for research aimed at using SI to treat RA.

Herbal self-assembled nanoplatforms (H-SANs) represent an emerging strategy in herbal nanomedicine by integrating the intrinsic bioactivity of phytochemica

Precision targeted delivery system based on nanomaterials is a feasible strategy to address anaphylaxis reactions of natural products. By loading sinomenine (SIN) into folate (FA) modified human serum albumin (HSA) nanomaterials, triple targeting including extravasation through leaky vasculature and subsequent Inflammatory cell-mediated sequestration (ELVIS) targeting, secreted protein acidic and rich in cysteine (SPARC) targeting and M1 macrophage targeting can be achieved, and the occurrence of anaphylaxis reactions can be reduced, so that SIN can be accurately delivered to rheumatoid arthritis (RA) joints. FA-SIN-HSA NPs exhibited potent anti-inflammatory activity and analgesic effect, and the possibility of inducing anaphylaxis reactions was extremely slight. FA-SIN-HSA NPs were also able to specifically target RA joints to prolong the circulating half-life of SIN as confirmed by highperformance liquid chromatography (HPLC) and in vivo fluorescence imaging. After collagen-II induced arthritis (CIA) mice were treated with FA-SIN-HSA NPs, the symptoms were greatly relieved, and the RA therapeutic effect was excellent. Taking this case as a reference, for anaphylaxis reactions of natural products, natural products can be loaded in nanomaterials modified with targeted modifiers to enhance the therapeutic effect and reduce anaphylaxis reactions.

Non‑small cell lung cancer (NSCLC) remains a leading cause of cancer‑associated mortality and urgently requires new therapeutic agents. In the present study, phenotypic screening of natural herbal extracts was performed, identifying Disporum cantoniense extract as a selective inhibitor of NSCLC cell viability. Bioactivity‑guided fractionation further revealed that the petroleum ether fraction (DPF) was the major active fraction. DPF suppressed the viability, proliferation, colony formation, migration and invasion of A549 and H1299 cells while exhibiting weaker cytotoxicity toward BEAS‑2B cells. In addition, DPF increased propidium iodide (PI)‑positive cell death and lactate dehydrogenase release in NSCLC cells, indicating that DPF‑induced viability loss was accompanied by membrane‑damaging cytotoxicity. Transcriptomic and network pharmacology analyses indicated significant enrichment of autophagy‑, apoptosis‑, AMPK‑, mTOR‑, and MAPK‑associated pathways. Mechanistically, DPF increased LC3‑II accumulation, promoted green fluorescent protein‑LC3 puncta formation and autophagic flux, and activated the AMPK/mTOR/unc‑51 like autophagy activating kinase 1 and MEK/ERK signaling pathways. DPF also induced apoptosis, as demonstrated by increased Annexin V positivity, elevated cleaved caspase‑3 and Bax expression, reduced Bcl‑2 expression, and reduced cytotoxicity in Bax‑Bak double‑knockout mouse embryonic fibroblast (MEF) cells. Notably, pharmacological inhibition of autophagy or its upstream regulators attenuated DPF‑induced cytotoxicity. In addition, autophagy‑deficient Atg7^‑/‑ MEF cells exhibited reduced DPF‑induced PI‑positive cell death, loss of cell viability, and caspase‑3 activation, further supporting the involvement of Atg7‑dependent autophagy in DPF‑induced apoptosis. In a xenograft model, DPF significantly inhibited tumor growth and increased apoptosis‑ and autophagy‑associated markers in tumor tissues without evident systemic toxicity. Collectively, these findings identify DPF as a principal anti‑NSCLC fraction of Disporum cantoniense and suggest that it suppresses NSCLC progression through AMPK/mTOR/unc‑51 like autophagy activating kinase 1‑ and MEK/ERK‑mediated autophagy‑dependent apoptosis.