Cigarette smoke induces persistent pulmonary inflammation and oxidative stress. Shenling Baizhu San (SLBZS) has shown anti-inflammatory activity, but its complex composition limits standardization. This study evaluated a SLBZS-derived defined-component formula (DCF) in rats during ongoing cigarette smoke exposure. Seventy male Sprague-Dawley rats were randomly assigned to seven groups (n = 10/group): control, model, dexamethasone, commercial SLBZS, and low-, medium-, and high-dose DCF groups. DCF was administered at approximately 2.75, 5.49, and 10.98 mg/kg/day, respectively. Except for controls, rats underwent cigarette smoke exposure for 120 min/day for 8 weeks, with drug administration initiated concurrently. Lung tissue levels of IL-1 β , IL-6, TNF- α , CXCL1, CCL2, 8-iso-PGF2 α , MDA, and SOD were measured. Lung histopathology and p-p38 and p-p53 protein levels were also assessed. Cigarette smoke exposure increased IL-1 β , IL-6, TNF-α, CXCL1, CCL2, and 8-iso-PGF2 α levels, reduced SOD activity, and increased p-p38 and p-p53 protein levels compared with controls ( p < 0.05 ). Medium- and high-dose DCF reduced these inflammatory and oxidative injury-related changes and improved histopathological abnormalities ( p < 0.05 ). MDA levels did not differ significantly among groups. Concurrent DCF administration attenuated cigarette smoke-induced lung inflammation and oxidative injury during continued smoke exposure. The accompanying reductions in p-p38 and p-p53 suggest possible involvement of related stress-response pathways, although causal pathway regulation was not established.
Paraquat (PQ) is a widely used herbicide with well-documented neurotoxic potential, largely associated with redox cycling, oxidative stress, and mitochondrial dysfunction. Excessive reactive oxygen species (ROS) generation following PQ exposure disrupts cellular redox homeostasis and contributes to neuronal cell injury. Vanillic acid (VA), a naturally occurring phenolic compound, has antioxidant and cytoprotective properties. This study investigated whether VA attenuates PQ-induced cellular toxicity and associated changes in oxidative status, mitochondrial membrane potential, cell-cycle distribution, and acetylcholinesterase (AChE) activity in SH-SY5Y human neuroblastoma cells. SH-SY5Y cells were exposed to PQ (100 µM) in the presence or absence of VA (10, 25, and 50 µM). Cell viability and membrane integrity were assessed using MTT and LDH assays, respectively. Oxidative stress parameters were evaluated by measuring intracellular ROS production, total antioxidant capacity (TAC), and total oxidant status (TOS). Mitochondrial membrane potential (ΔΨm) was analyzed using JC-1 staining, and cell-cycle distribution was determined by flow cytometry. Acetylcholinesterase (AChE) activity was measured to assess PQ-associated cholinergic alterations. PQ exposure significantly reduced cell viability and TAC while increasing LDH release, ROS production, TOS, mitochondrial depolarization, and AChE activity. PQ exposure was also associated with an increased Sub-G1 population and altered cell-cycle distribution. Co-treatment with VA concentration-dependently improved viability and membrane integrity, reduced ROS and TOS, partially restored TAC, decreased mitochondrial depolarization, attenuated cell-cycle alterations, and reduced PQ-associated AChE elevation. In SH-SY5Y cells, VA attenuated PQ-induced cellular toxicity and was associated with improved redox indices, reduced mitochondrial depolarization, and modulation of AChE activity. These functional findings support a potential cytoprotective effect of VA, but the responsible molecular pathways, apoptosis, and direct cholinergic function require confirmation in differentiated neuronal models and by pathway-specific assays.
Colorectal cancer represents a significant global health burden, standing as the third most frequently diagnosed malignancy and the second leading cause of cancer-related fatalities worldwide. This highlights the urgent need for new and innovative therapeutic agents. This study aimed to investigate the anticancer effects of postbiotic derived from Bacillus coagulans GBI-30,6086 and investigate their impact on the mRNA expression of key candidate genes associated with colorectal cancer signaling networks. The postbiotic was extracted and its antimicrobial activity and physicochemical characteristics was evaluated using FTIR spectroscopy. The anti-proliferative and apoptotic effects of the postbiotic on Caco-2 (cancerous) and HDF (General non-cancerous human cell model) cells were assessed through MTT and Annexin V/PI flow cytometry assays. At the molecular level, relative mRNA expression changes across 12 candidate genes involved in apoptosis, proliferation, and inflammation were quantified using RT-qPCR, complemented by KEGG pathway mapping analysis. The postbiotic exerted dose and time dependent cytotoxic effects on Caco-2 cells while showing high biocompatibility toward healthy HDF cells. Flow cytometry confirmed a significant, selective induction of programmed cell death in malignant cells. At the transcriptomic level, postbiotic treatment significantly upregulated the tumor suppressor PTEN and the pro-apoptotic gene CASP9, while downregulating PIK3CB, BCL2, TLR4, TGFB, EGFR, GLI2, and CEACAM5. Expression shifts for CTNNB1, HES1, and IL6 demonstrated downward trends without reaching statistical significance. KEGG pathway mapping confirmed the functional integration of these candidate genes within central cascades, including Pathways in cancer and Colorectal cancer. Our findings indicate that B. coagulans GBI-30 postbiotic exert selective cytotoxicity and induce apoptosis in Caco-2 cells, accompanied by distinct transcriptomic modulation of key oncogenic and inflammatory gene markers. These results highlight the biotherapeutic potential of postbiotics as a safe candidate for complementary cancer management, warranting further functional protein-level investigation.
Patellofemoral pain syndrome (PFPS) is a prevalent knee disorder involving quadriceps dysfunction, proximal hip control deficits, and myofascial trigger points (MTrPs). Although dry needling is increasingly used as an adjunct intervention, evidence on its efficacy for correcting neuromuscular deficits—particularly the hamstring-to-quadriceps (H/Q) peak torque ratio—remains limited. This study aimed to determine whether dry needling targeting MTrPs in the quadriceps, hip adductors, and tensor fasciae latae combined with home stretching is superior to sham needling plus stretching in improving pain, function, and the H/Q ratio. This was a randomised, single-blind, sham-controlled superiority trial. Sixty-six participants with PFPS were randomly assigned 1:1 to active dry needling of MTrPs plus home stretching (n = 33) or sham superficial needling at non-trigger point sites plus identical stretching (n = 33). Interventions were delivered once weekly for six weeks. Primary outcomes were pain intensity (Visual Analogue Scale, VAS) and knee function (Lysholm Knee Scoring Scale, LKSS) assessed at baseline, week 8, and six-month follow-up. Secondary outcomes included active knee flexion range of motion, pressure pain threshold, isokinetic quadriceps and hamstring peak torque, and the H/Q ratio, assessed at baseline and week 8. At week 8, the dry needling group showed significantly greater improvements in pain (mean difference − 1.18, 95
Periodontitis is a chronic inflammatory disease induced by microbial biofilm dysbiosis and aberrant host immune responses, leading to progressive alveolar bone resorption. Traditional Chinese Medicine (TCM) offers multi-target therapeutic strategies for managing inflammatory diseases. This study aimed to investigate the anti-inflammatory potential of Tryptanthrin, a candidate bioactive constituent of Yinhuang Gargle, our hospital’s empirical formula (composed of Scutellariae Radix (10 g), Phellodendri Chinrnsis Cortex (10 g), Lonicerae Japonicae Flos (5 g), Isatidis Folium (8 g), Agrimonia Eupatoria (5 g), and licorice (3 g)), for treating periodontitis using network pharmacology, molecular docking, molecular dynamics simulation, and in vitro experimental methods. Pharmacological databases were utilized to screen the active components of the formula. Potential action targets were predicted and intersected with targets from periodontitis-related disease databases. A protein-protein interaction (PPI) network was constructed to identify core targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Molecular docking and molecular dynamics simulation was employed to verify the interactions between key active compounds and core targets. Finally, the anti-inflammatory effects of the core compound Tryptanthrin were validated through in vitro cell experiments. Network pharmacology analysis revealed that the formula likely exerts its effects by modulating key targets such as TNF-α, AKT1, BCL2, IL-6, and NFKB1, which are involved in inflammatory responses, oxidative stress, and osteoclastogenesis. Inflammatory signaling pathways including the TNF-α/NF-κB network were identified as core pathways. Molecular docking confirmed strong binding affinity between the bioactive compounds and these core targets. Molecular dynamics simulations revealed the multifaceted binding stability between Tryptanthrin and BCL2. In vitro experiments further validated that Tryptanthrin not only reduces the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) but also downregulates LPS‑induced upregulation of iNOS and COX‑2 at the protein level, further supporting its anti‑inflammatory mechanism. This study identifies Tryptanthrin as a promising antiinflammatory candidate for periodontitis, and offers a valuable paradigm for mechanismbased discovery of bioactive constituents from TCM formulas through the integration of network pharmacology, molecular docking, and in vitro experimental.
