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This study aimed to evaluate the clinical application of different myopia correction methods in the prevention and control of myopia in adolescents. A total of 145 myopic adolescents aged 8 to 15 years were included, and their eyes were divided into four groups based on the treatment modality: wearing Defocus Incorporated Multiple Segments (DIMS) spectacle lenses alone (Group A), orthokeratology (OK) lenses alone (Group B), DIMS spectacle lenses combined with racemic anisodamine eye drops (Group C), and OK lenses combined with racemic anisodamine eye drops (Group D). The primary outcomes, including axial length and refractive error (expressed as spherical equivalent refraction, SER), were measured at baseline and at the 12-month follow-up. The clinical effects of each group were compared. The results showed significant differences in myopia progression across the groups, with Group D showing the least axial elongation. OK lenses were more effective than DIMS spectacle lenses in controlling myopia progression, and the combination of racemic anisodamine eye drops further enhanced the correction effect. This study provides important clinical evidence for myopia control interventions in adolescents.

Background Septic shock is characterized by an uncontrolled inflammatory response and microcirculatory dysfunction. There is currently no specific agent for treating septic shock. Anisodamine is an agent extracted from traditional Chinese medicine with potent anti-inflammatory effects. However, its clinical effectiveness remains largely unknown. Methods In a multicentre, open-label trial, we randomly assigned adults with septic shock to receive either usual care or anisodamine (0.1–0.5 mg per kilogram of body weight per hour), with the anisodamine doses adjusted by clinicians in accordance with the patients’ shock status. The primary end point was death on hospital discharge. The secondary end points were ventilator-free days at 28 days, vasopressor-free days at 28 days, serum lactate and sequential organ failure assessment (SOFA) score from days 0 to 6. The differences in the primary and secondary outcomes were compared between the treatment and usual care groups with the χ 2 test, Student’s t test or rank-sum test, as appropriate. The false discovery rate was controlled for multiple testing. Results Of the 469 patients screened, 355 were assigned to receive the trial drug and were included in the analyses—181 patients received anisodamine, and 174 were in the usual care group. We found no difference between the usual care and anisodamine groups in hospital mortality (36% vs. 30%; p  = 0.348), or ventilator-free days (median [Q1, Q3], 24.4 [5.9, 28] vs. 26.0 [8.5, 28]; p  = 0.411). The serum lactate levels were significantly lower in the treated group than in the usual care group after day 3. Patients in the treated group were less likely to receive vasopressors than those in the usual care group (OR [95% CI] 0.84 [0.50, 0.93] for day 5 and 0.66 [0.37, 0.95] for day 6). Conclusions There is no evidence that anisodamine can reduce hospital mortality among critically ill adults with septic shock treated in the intensive care unit. Trial registration ClinicalTrials.gov ( NCT02442440 ; Registered on 13 April 2015).

Postoperative nausea and vomiting (PONV) frequently occur in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) under general anesthesia. Glycopyrronium bromide, an anticholinergic medication, is believed to not only relieve gastrointestinal spasms but also effectively prevent PONV. To compare the incidence of nausea and vomiting and the effect of relieving spasm between patients administered glycopyrronium bromide and those given anisodamine hydrobromide following endoscopic retrograde cholangiopancreatography (ERCP). This is a monocentric prospective study. Patients eligible for ERCP were randomly assigned to two groups. One group received 0.2 mg glycopyrronium bromide (Group G) intravenously, while the other group received 10 mg anisodamine hydrobromide (Group A) intramuscularly for anesthesia induction. The study assessed duodenal motility during ERCP and the incidence of PONV within 24 hours. The study included 130 patients. Nausea and vomiting within 24 hours post-surgery occurred in nine patients (13.8%) in Group G and 19 patients (29.2%) in Group A, with statistical significance (relative risk (RR), 0.47; 95% confidence interval (CI) [0.02-0.29];  = 0.033). Vomiting specifically was observed in three patients (4.6%) in Group G and 12 patients (18.5%) in Group A, showing statistical significance (RR 0.25; 95% CI [0.03-0.25];  = 0.028). There was no significant difference in duodenal peristalsis between the groups (Group G: 10.9 ± 3.1 times/min; Group A: 11.6 ± 3.1 times/min;  = 0.174). For patients undergoing ERCP under general anesthesia, a subcutaneous injection of 0.2 mg glycopyrronium bromide significantly reduces PONV and provides similar anti-spasmodic effects to 10 mg intramuscular anisodamine hydrobromide.

The objective of this study is to observe the effects of high dose of anisodamine in the respiratory function of patients with acute lung injury (ALI) induced by trauma. Fifty cases of patients with complicated ALI after trauma were randomly divided into the anisodamine treatment group ( n  = 26) and the conventional treatment group ( n  = 24). Intravenous injection of high dose of anisodamine was administrated in the anisodamine treatment group on the basis of conventional treatment. Acute lung injury scores, oxygenation index, PaO 2 , respiratory mechanic index, mechanical ventilation time, and the occurrence of adverse reactions in the two groups were observed. Acute lung injury scores and respiratory parameters were all significantly improved in the two groups of patients after the treatment ( P   <  0.05); compared with the conventional treatment group, the improvements of respiratory function in the anisodamine treatment group were more obvious ( P  < 0.05), the mechanical ventilation time was shorter ( P  < 0.05), and there was no significant adverse reaction. In conclusion, high dose of anisodamine contributed to improve the respiratory function of the patients with traumatic ALI.

Sepsis, marked by hyperinflammation and subsequent immunosuppression, lacks effective phase-specific therapies. Although anisodamine hydrobromide (Ani HBr) reduced 28-day mortality in our prior trial, its mechanisms remained unclear. Here, we integrated network pharmacology, machine learning, immunological profiling, molecular simulations, and single-cell transcriptomics to elucidate Ani HBr’s multi-target actions. Among 30 cross-species targets, ELANE and CCL5 emerged as core regulators via protein interaction networks, survival modeling (AUC: 0.72–0.95), and statistical significance (p < 0.05). Ani HBr inhibited ELANE-driven NET formation (HR = 1.176), associated with immunosuppression and endothelial damage, while enhancing CCL5-related cytotoxic T-cell recruitment (HR = 0.810). Docking and dynamics simulations showed Ani HBr binds ELANE’s catalytic cleft, suggesting direct inhibition of its enzymatic activity, and interacts stably with CCL5 at potential receptor-binding interfaces, indicating a modulatory role. Single-cell analysis revealed ELANE upregulation in CCI-phase neutrophils and widespread yet stage-specific CCL5 expression. These findings support Ani HBr as a phase-tailored agent that targets ELANE in early hyperinflammation while preserving CCL5-mediated immunity. The ELANE/CCL5 prognostic model offers a framework for precision immunotherapy in sepsis.

Lung cancer is the most common cancer and the leading cause of cancer deaths worldwide. We previously showed that solamargine, one natural phytochemicals from traditional plants, inhibited the growth of lung cancer cells through inhibition of prostaglandin E2 (PGE2) receptor EP4. However, the potential downstream effectors of EP4 involving in the anti‐lung cancer effects of solamargine still remained to be determined. In this study, we further verified that solamargine inhibited growth of non‐small‐cell lung cancer (NSCLC) cells in multiple cell lines. Mechanistically, solamargine increased phosphorylation of ERK1/2. Moreover, solamargine inhibited the protein expression of DNA methyltransferase 1 (DNMT1) and c‐Jun, which were abrogated in cells treated with MEK/ERK1/2 inhibitor (PD98059) and transfected with exogenously expressed DNMT1 gene, respectively. Interestingly, overexpressed DNMT1 gene antagonized the effect of solamargine on c‐Jun protein expression. Intriguingly, overexpressed c‐Jun blocked solamargine‐inhibited lung cancer cell growth, and feedback resisted the solamargine‐induced phosphorylation of ERK1/2. A nude mouse xenograft model implanted with lung cancer cells in vivo confirmed the results in vitro. Collectively, our results show that solamargine inhibits the growth of human lung cancer cells through reduction of EP4 protein expression, followed by increasing ERK1/2 phosphorylation. This results in decrease in DNMT1 and c‐Jun protein expressions. The inter‐correlations between EP4, DNMT1 and c‐Jun and feedback regulation of ERK1/2 by c‐Jun contribute to the overall responses of solamargine in this process. This study uncovers an additional novel mechanism by which solamargine inhibits growth of human lung cancer cells.

Anisodamine is an ancient Chinese medicine derived from Tibet as a belladonna alkaloid, which is usually used for improvement of blood circulation in patients with organ phosphorus poisoning or shock. In this study, for the first time, we report its cardioprotective effects on preventing ischemia/reperfusion (I/R) injury of patients with acute myocardial infarction (AMI), and decreasing the myocardial infarction area and severity in heart of Sprague–Dawley (SD) rats. Our results suggest a potential molecular mechanism of anisodamine against the I/R injury in cardiomyocytes is associated with its anti-apoptotic effect. Anisodamine treatment decreases the expression of caspase-3 and caspase-8, and increases Bcl-2/Bax ratio in cardiomyocytes. Our data suggest that anisodamine can provide significant cardioprotection against I/R injury, potentially through the suppression of cardiomyocytes apoptosis.

The aim of the present study was to investigate the cardioprotective effects of anisodamine against myocardial ischemia/reperfusion (I/R) injury and the molecular mechanisms involved. The present results demonstrated that anisodamine attenuated myocardial infarct sizes, decreased the levels of creatine kinase and lactate dehydrogenase, whereas it increased the left ventricular (LV) systolic pressure, the LV end-diastolic pressure, and the LV pressure maximum rising and falling rates in a myocardial I/R rat model. In addition, anisodamine was revealed to suppress oxidative stress, inflammatory factor production and myocardial cell apoptosis, as demonstrated by the downregulation of caspase-3 and apoptosis regulator BAX protein expression. The production of reactive oxygen species was decreased and the protein expression of inducible nitric oxide synthase (iNOS) was downregulated, whereas the expression of endothelial NOS was enhanced. In addition, the activity of nicotinamide-adenine dinucleotide phosphate oxidase (Nox) was suppressed and the expression of Nox4 was downregulated in rats with myocardial I/R injury. In conclusion, the results of the present study suggested that anisodamine exerted a cardioprotective effect against myocardial I/R injury in rats, through the inhibition of oxidative stress, the suppression of inflammatory processes and the inhibition of myocardial cell apoptosis.

Background/Aims: Solamargine, one natural photochemical component from traditional plants, has been shown to have anti-cancers properties. We previously showed that solamargine inhibited the growth of non-small-cell lung cancer (NSCLC) cells through suppression of prostaglandin E2 (PGE 2 ) receptor EP4 gene and regulation of downstream signaling pathways. However, the detailed mechanism underlying this, especially in combination of metformin, a known AMPK activator, still remained to be determined. Methods: Cell viability was measured using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and colorimetric 5-bromo-2-deoxyuridine (BrdU) ELISA methods, respectively. Western blot analysis and immunohistochemistry were performed to examine the phosphorylation and protein expressions of signal transducer and activator of transcription 3 (Stat3), SP1, forkhead box O3a (FOXO3a), and insulin-like growth factor (IGF)-IGF binding protein 1 (IGFBP1). The expression of IGFBP1 mRNA was measured by quantitative real time PCR (qRT-PCR). Silencing of FOXO3a and IGFBP1 were examined by siRNA procedures. Exogenously expression of SP1, FOXO3a, and IGFBP1 were carried out by transient transfection assays. The promoter activity of IGFBP1 was tested using Secrete-Pair TM Dual Luminescence Assay Kit. A xenografted tumor model was used to further test the effect of solamargine in combining with metformin in vivo. Results: We further demonstrated that solamargine inhibited growth and induced cell cycle arrest in other NSCLC cell lines. Through mechanism-based approaches, we showed that solamargine decreased the phosphorylation of Stat3; In addition, solamargine induced FOXO3a, whereas reduced SP1 protein levels; all of which were abrogated in cells with overexpressed Stat3 gene. Interestingly, there is interaction between FOXO3a and SP1. Moreover, solamargine increased mRNA, protein expression and promoter activity of IGFBP1, which was not observed in cells with overexpressed SP1 or with silenced FOXO3a genes. Finally, ablation of IGFBP1 expression by siRNA blocked the effect of solamargine on cell growth inhibition. More importantly, there was a synergy of combination of solamargine and metformin. Similar findings were also observed in vivo. Conclusion: Our results show that solamargine increases IGFBP1 gene expression through inactivation of Stat3, followed by regulation and reciprocal interaction of FOXO3a and SP1 in vitro and in vivo. This ultimately leads to suppression of human lung cancer cell growth. Moreover, this is a synergy of solamargine in combination with metformin in this process. This study unravels a novel mechanism underlying the anti-lung cancer effects of solamargine in combination of metformin, and suggests a potential new lung cancer associated therapy.

Motion sickness presents a challenge due to its high incidence and unknown pathogenesis although it is a known fact that a functioning vestibular system is essential for the perception of motion sickness. Recent studies show that the efferent vestibular neurons contain calcitonin gene-related peptide (CGRP). It is a possibility that the CGRP immunoreactivity (CGRPi) fibers of the efferent vestibular system modulate primary afferent input into the central nervous system; thus, making it likely that CGRP plays a key role in motion sickness. To elucidate the relationship between motion sickness and CGRP, the effects of CGRP on the vestibular efferent nucleus and the vestibular nucleus were investigated in rats with motion sickness. An animal model of motion sickness was created by subjecting rats to rotary stimulation for 30 minutes via a trapezoidal stimulation pattern. The number of CGRPi neurons in the vestibular efferent nucleus at the level of the facial nerve genu and the expression level of CGRPi in the vestibular nucleus of rats were measured. Using the ABC method of immunohistochemistry technique, measurements were taken before and after rotary stimulation. The effects of anisodamine on the expression of CGRP in the vestibular efferent nucleus and the vestibular nucleus of rats with motion sickness were also investigated. Both the number of CGRPi neurons in the vestibular efferent nucleus and expression level in the vestibular nucleus increased significantly in rats with motion sickness compared to that of controls. The increase of CGRP expression in rats subjected to rotary stimulation 3 times was greater than those having only one-time stimulation. Administration of anisodamine decreased the expression of CGRP within the vestibular efferent nucleus and the vestibular nucleus in rats subjected to rotary stimulation. In conclusion, CGRP possibly plays a role in motion sickness and its mechanism merits further investigation.