Alcoholic liver disease (ALD) poses a significant global health challenge by causing progressive damage due to excessive alcohol consumption, highlighting the urgent need for effective treatments. Jin Ge Fang (JGF) is a traditional formulation whose potential hepatoprotective mechanism remains to be fully elucidated. This study aimed to investigate the protective effects of JGF on ALD and explore its regulatory roles in oxidative stress, inflammatory cascades, and the Toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway. An ethanol-induced ALD rat model was established and assessed histopathologically. Serum levels of hepatic function markers [aspartate transaminase (AST) and alanine transaminase (ALT)] and oxidative stress indicators [malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px)] were measured. Inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)] were quantified using enzyme-linked immunosorbent assay (ELISA). Protein expression related to the TLR4/NF-κB pathway was analyzed by Western blotting. JGF treatment significantly improved liver histology, reducing steatosis and inflammatory infiltration. It markedly decreased serum AST and ALT activities, suppressed lipid peroxidation (as evidenced by reduced MDA levels), and enhanced endogenous antioxidant defenses (elevated SOD and GSH-Px activities). Furthermore, JGF significantly inhibited the release of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and downregulated the protein expression of key mediators in the TLR4/NF-κB signaling pathway. JGF demonstrates significant hepatoprotective effects against ALD. Its benefits are likely mediated through a dual action of ameliorating oxidative damage and suppressing inflammatory activation, potentially via inhibition of the TLR4/NF-κB signaling cascade.

Myocardial ischemia-reperfusion (I/R) injury represents a critical complication in cardiovascular diseases, profoundly influencing patient prognosis. This study endeavors to elucidate the protective mechanisms and effects of Platycodin-D (PD) on myocardial ischemia-reperfusion injury (MIRI). A rat model of myocardial ischemia-reperfusion was employed to assess the impact of PD treatment on cardiac performance, myocardial injury biomarkers (CK-MB, LDH, cTnI), and infarct size. Further mechanistic insights were gained through Western blot and JC-1 staining, which analyzed the modulation of the HIF-1α/BNIP3 signaling pathway and mitochondrial autophagy by PD. PD treatment markedly improved cardiac function, decreased levels of myocardial injury biomarkers (CK-MB, LDH, cTnI), and reduced infarct size. Mechanistically, PD was found to regulate the HIF-1α/BNIP3 signaling pathway, inhibit mitochondrial autophagy, and enhance mitochondrial function. Western blot and JC-1 staining confirmed that PD increases mitochondrial membrane potential and reduces the number of damaged mitochondria in cardiomyocytes. This study underscores the significant protective effects of Platycodin-D against myocardial ischemia-reperfusion injury, presenting a promising therapeutic approach for cardiovascular disease management.

Paraquat (PQ) poisoning causes acute pulmonary injury via oxidative stress and epithelial-mesenchymal transition (EMT), with limited treatment options. This study investigated whether andrographolide (Andro) alleviates PQ-induced lung damage and the underlying mechanisms. PQ-induced pulmonary injury was established in C57BL/6J mice. Animals were assigned to Control, Andro, PQ and PQ +Andro groups. Lung pathology, oxidative stress markers (MPO, ROS, MDA, SOD, CAT), EMT markers (E-cadherin, α-SMA), and PI3K/Akt/PPARγ pathway proteins were assessed in vivo and in MLE-12 cells, with PI3K inhibition using LY294002. Andro significantly improved survival, reduced alveolar injury and collagen deposition, and suppressed oxidative stress by downregulating ROS/MDA/MPO and enhancing SOD/CAT. It suppressed EMT by upregulating E-cadherin and reducing α-SMA. Andro inhibited PI3K/Akt activation and increased PPARγ expression. LY294002 partially reproduced these effects, supporting pathway involvement. Andro mitigates PQ-induced lung damage by limiting oxidative stress and EMT via the PI3K/Akt/PPARγ pathway. These findings provide preclinical evidence for its further investigation as a candidate protective agent.

One of the most common diseases in the world is sinusitis, which is an inflammation of the membranes lining the paranasal sinuses. The bacteria involved are highly resistant to antibiotics, prompting scientists to explore green bioactives as potential biofilm inhibitors. The current study investigated the antioxidant potential, phytochemical screening, antibacterial and biofilm inhibition potential of polyherbal extracts prepared using distilled water, ethanol, hydroethanol and n-hexane solvents. However, no prior research has specifically addressed their use in treating sinusitis. Samples were prepared by maceration method followed by antioxidant and phytochemical analysis. Chemical fingerprinting was conducted using FTIR, GC-MS and LC-MS analysis. Antibacterial activity, Minimum inhibitory concentration (MIC) and biofilm inhibition was checked. Among the extracts, polyherbal ethanol extract showed the highest antioxidant activity, followed by n-hexane, distilled water and hydroethanol. The distilled water extract showed the highest flavonoid and phenolic content, followed by hydroethanol. Different functional groups were identified in all extracts. Bioactive compounds such as quercitrin and kaempferol derivatives were identified. Antibacterial profile showed that hydroethanol extract was the most effective against sinusitis isolates (Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus aureus and Enterococcus faecalis) with the lowest MIC against Proteus mirabilis. Biofilm inhibition assay revealed the highest inhibition by hydroethanol extract against E. faecalis followed by ethanol extract against E. coli. The findings suggest that polyherbal extracts, particularly in hydroethanol and ethanol, possess significant antioxidant, antibacterial and biofilm inhibiting properties and could serve as promising candidates for the effective management of sinusitis.

Edaravone can reduce damage to brain cells in a variety of ways. Rho/ROCK signaling is involved in Alzheimer's disease. This study uses AD cell models to explore edaravone's effect on AD nerve synapse damage. The ROCK2 promoter luciferase reporter gene was constructed, Aβ25-35 was used as a processing factor and transfected into PC12 cells to construct an AD cell model which was then treated with edaravone, followed by analysis of 95 antibody (PSD95), synapse-related mRNA synapsin 1 (SYN1) level to observe its effect on Rho/ROCK signaling. Edaravone can effectively inhibit the transcriptional activity of ROCK2 promoter in AD cell model, upregulate SYN1 and GAP43 protein and downregulate ROCK2. After ROCK2 overexpression, edaravone can affect SYN1 expression in AD cell model, while SYN1 expression did not change significantly after ROCK2 was silenced. Edaravone has a protective effect on AD nerve synapse damage and plays a role in repairing nerve synapse damage through ROCK2 signaling pathway.

Curcumin exhibits limited oral bioavailability owing to its poor solubility and rapid metabolism. To develop a novel curcumin nano-gel (CNG) and evaluate its pharmacokinetics following oral and rectal administration. A sensitive LC MS/MS method was established for the simultaneous quantification of curcumin and its major metabolite curcumin O glucuronide (COG) in plasma. The pharmacokinetics of CNG were compared with those of curcumin suspension (CS) to evaluate the improvement in oral and rectal absorption. CNG and curcumin suspension (CS) were administered orally (1000 mg/kg) and rectally (200 mg/kg) to mice or rats. Plasma samples were collected, and pharmacokinetic parameters were analyzed using WinNonlin. CNG formed well dispersed nanoparticles in water. Oral administration of CNG significantly enhanced curcumin absorption, yielding a 66.7 fold higher Cmax for curcumin and an 84.8 fold higher Cmax for COG compared with CS. The AUC of curcumin and COG increased by 9.2 fold and 24.4 fold, respectively. Rectal administration of CNG resulted in a 5.5 fold higher Cmax and a 3.5 fold higher AUC of curcumin relative to oral CS. CNG markedly improves the bioavailability of curcumin via both oral and rectal routes, demonstrating its potential as an effective delivery system for enhancing curcumin therapeutic application.

Congenital Adrenal Hyperplasia (CAH) is a group of disorders characterized by impaired adrenal steroid hormone synthesis, with a wide spectrum of clinical manifestations. The prognosis of CAH depends on factors, such as clinical phenotype, treatment and management. To analyze the factors influencing the quality of life in children with CAH. This retrospective study included 30 CAH patients divided into good prognosis (n=13) and poor prognosis (n=17) groups. Clinical characteristics, genetic mutations, treatment compliance, medication regimens and complications were analyzed by t-tests and logistic regression. The good prognosis group presented better compliance (92.31% vs. 47.06%, P=0.017) and hormonal control (84.62% vs. 35.29%, P=0.01). The prevalence of the salt-wasting (SW) type of CAH was higher in the poor prognosis group (70.59% vs. 23.08%, P=0.038), while the simple virilizing (SV) type was higher in the good prognosis group (53.85% vs. 17.65%). The poor prognosis group received a higher hydrocortisone dose (16±3mg/m2/day) compared to the good prognosis group (12±4mg/m2/day, P=0.025). Complications such as hypertension (P=0.017), hyperpigmentation (P=0.026) and urinary incontinence (P=0.017) were more prevalent in the poor prognosis group. In children with CAH, the quality of life is significantly affected by treatment compliance, hormonal control, and the presence of complications.

Studies have confirmed that the progression of sepsis is closely related to intestinal barrier dysfunction, including intestinal mucosa ischemia and hypoxia, flora imbalance and epithelial cell apoptosis. Therefore, protecting the intestinal barrier function has become a key link in the comprehensive treatment of sepsis. This study evaluated the impact of a novel β-lactamase inhibitor compound preparation (ceftazidime/avibactam) on intestinal barrier function in sepsis patients. The study included 108 sepsis patients (January 2022‒August 2025) and grouped them as an observation group (54 cases, ceftazidime/avibactam+dynamic nutritional support) and a control group (54 cases, Ceftazidime/Sulbactam+dynamic nutritional support). Of the outcome measures assessed, the 28-day all-cause mortality was primary, while ICU length of stay, mechanical ventilation time, antibiotic course, intestinal barrier function markers (DAO, LBP, Claudin-1) and inflammatory cytokines (IL-6, TNF-α) were secondary. The results indicated lower 28-day all-cause mortality in the observation group vs the control group, along with shorter ICU length of stay, mechanical ventilation time and time to negative blood culture conversion (P<0.05). Concerning post-treatment intestinal barrier function, DAO, LBP and FC were lower while claudin-1 was higher in the observation group compared to the control group (P<0.05). Analysis of inflammatory factors also showed greater reductions in IL-1β, IL-6 and TNF-α in the observation group post-treatment (P<0.05). Ceftazidime/Avibactam plus dynamic nutritional support is instrumental in improving the intestinal barrier function of sepsis patients and alleviating inflammatory reactions, thus enhancing life safety.

Post-herpetic neuralgia (PHN) is a common refractory complication of herpes zoster, characterized by persistent neuropathic pain that seriously impairs patients' quality of life. The study aimed to assess the clinical effects of gabapentin when administered in combination with Hegu-point catgut embedding in patients suffering from post-herpetic neuralgia (PHN). A randomized, assessor-blinded study was conducted, wherein a total of 210 PHN patients were equally divided into two groups: 1) the control group receiving only gabapentin and 2) the combination group that received combined therapy of gabapentin and Hegu-point catgut embedding weekly. After 4 weeks of treatment, pain intensity, sleep quality, serum biomarkers, clinical efficacy and adverse events were evaluated. After 4 weeks, both groups displayed a significant reduction in Visual Analogue Scale (VAS) and Pittsburgh Sleep Quality Index (PSQI) scores, with greater improvement reported in the combination group (P < 0.05). In addition, both groups showed a significant decrease in serum levels of substance P, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), while β-endorphin levels showed a significant increase. The changes were found to be more pronounced in the combination group (P < 0.05). Interestingly, the combination group demonstrated a higher overall response rate (92.38% vs 80.00%) and fewer adverse events (12.38% vs 26.67%, P < 0.05). Altogether, combination therapy provided superior short-term improvement in symptoms and biomarker modulation as compared to gabapentin alone. Since the present study only assessed peripheral serum markers, the underlying mechanistic pathways could not be deciphered. Additionally, longer-term outcomes of therapy were not assessed, serving as a major limitation of this study.

Patients with diabetes mellitus combined with hypertension and coronary artery disease (DM-HTN-CAD) are prone to QTc interval prolongation and ventricular arrhythmia. Although sodium glucose cotransporter-2 (SGLT2) inhibitors have hypoglycemic and cardioprotective effects, their regulatory effects on relevant indicators in such patients still need to be clarified. This study aimed to analyze the impact of SGLT2 inhibitor on QTc interval and ventricular arrhythmia in patients with DM-HTN-CAD. From January 2023 to January 2025, 150 patients with DM-HTN-CAD were selected in the Hospital. Patients were divided into conventional treatment and SGLT2 inhibitor groups depending on the treatment regimen. The SGLT2 inhibitors group received SGLT2 inhibitor treatment in addition to the conventional treatment group. Compression of the main indicators [including QTc interval, changes in echocardiographic parameters (left and right ventricular diameter, left and right atrial diameter and ejection fraction), blood pressure and glucose indicators] and secondary indicators (including quality of life score, incidence of complications and incidence of adverse reactions) before and after treatment was done among both groups. No differences were observed in the basic characteristics between the two groups (P>0.05). After treatment, all parameters between the two groups illustrated a remarkable discrepancy compared with pre-treatment (P<0.05). In addition, patients in the SGLT2 inhibitors group exhibited lower QTc intervals, left and right atrial diameters, left and right ventricular diameters, systolic blood pressure, diastolic blood pressure and fasting blood glucose levels as compared to the conventional therapy group; The left ventricular ejection fractions, quality of life scores and overall clinical response rates were higher (P<0.05). The complications and adverse reaction incidences were lower in the SGLT2 inhibitors group compared to the conventional treatment group (P<0.05). SGLT2 inhibitors effectively shorten QTc interval, reduce ventricular arrhythmia and cardiovascular risks in DM-HTN-CAD patients and show favorable safety for clinical reference.