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betamethasone dipropionate + salicyclic acid (Diprosalic)

✓ Approved

Merck & Co. · PTGS1 · 小分子

什么是 betamethasone dipropionate + salicyclic acid？

betamethasone dipropionate + salicyclic acid 是一种小分子，由Merck & Co.研发。该药已获批，用于治疗相关适应症，给药途径：Topical。

药物档案

商品名Diprosalic
公司Merck & Co.
药物类别小分子
分子靶点PTGS1, PTGS2, TBXAS1
给药途径Topical
状态Approved
来源： ClinicalTrials.gov, Merck & Co.

作用机制

分子靶点

betamethasone dipropionate + salicyclic acid 作用于 3 个分子靶点：

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
PTGS2prostaglandin-endoperoxide synthase 2 (GRIPGHS, hCox-2)
TBXAS1thromboxane A synthase 1 (CYP5, TXS)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

betamethasone dipropionate + salicyclic acid 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersEczema✓ Approved
Hepatobiliary disordersHepatitis✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

相关研究文献

PubMedPhysiological reports2026-09-11

Fatty acid species differentially regulate macrophage polarization and oxidative stress with secondary effects on macrophage-HSC crosstalk.

Nakanishi Koichi K, Shinkawa Hiroji H, Takemura Shigekazu S, Nakagawa Kanako K et al.

Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by lipid accumulation, inflammation, and fibrosis. Macrophage-hepatic stellate cell (HSC) communication plays a key role in fibrogenesis; however, how fatty acid species influence macrophage polarization remains unclear. Bone marrow-derived macrophages (BMDMs) were polarized toward M1 or M2 phenotypes in the presence of palmitic acid (PA), oleic acid (OA), or palmitoleic acid (PO). Polarization markers, reactive oxygen species (ROS), and peroxisome proliferator-activated receptor gamma (PPARγ) expression were analyzed by RT-qPCR, Western blotting, and chemiluminescence. Primary HSCs were exposed to fatty acids or conditioned media from treated macrophages. PA enhanced selected inflammatory macrophage responses and increased ROS production under M1-polarizing conditions. OA enhanced ROS production in M1 macrophages and suppressed several M2-associated markers, whereas PO reduced inflammatory responses and ROS under M1-polarizing conditions. Direct fatty acid exposure did not significantly alter HSC activation markers. Conditioned media from polarized macrophages, particularly M1 macrophages, reduced α-SMA and cytoglobin protein expression in HSCs, while fatty acid-specific effects were modest and marker-dependent. Fatty acid species differentially modulate macrophage polarization and redox activity, partly in association with PPARγ signaling. These macrophage changes may secondarily affect macrophage-HSC communication and stellate cell redox-related responses, providing insight into lipid regulation of immune-stromal interactions in the liver.

PMID 42723224
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PubMedFrontiers in plant science2026-09-11

Comparison of heavy metal contents, fatty acid composition, and palinological characteristics of two different Hypericum species growing in mining-impacted area.

Ahıskalı Mihriban M

This study comparatively evaluated heavy metal (Al, Cd, Cr, Fe, and Mn) concentrations, fatty acid composition, and palynological characteristics in Hypericum scabrum and Hypericum lydium samples collected from mining-impacted and reference sites of an iron ore operation. Plant samples of H. scabrum and H. lydium were collected from mining-impacted and reference sites in Bingöl Province, Türkiye. Heavy metal concentrations, fatty acid composition, and pollen morphological characteristics were analyzed using ICP-MS, gas chromatography, and light microscopy, respectively. Translocation factor (TF) and statistical analyses were also performed. In both species, Al, Cr, Fe, and Mn accumulation was markedly increased in the mining area, whereas the increase in Cd remained relatively limited with statistically significant differences between sites. Translocation factor (TF) analyses revealed higher values for most metals in the mining area; notably, H. lydium exhibited a greater translocation capacity for Fe and Mn. In contrast, TF values for Cr remained below 1 in both species, indicating its retention at the root level. Mining conditions were found to markedly alter the fatty acid composition in both Hypericum species, particularly affecting the balance between saturated and unsaturated fatty acids. Under heavy metal stress, total saturated fatty acids (ΣTSFA; particularly palmitic acid (C16:0) and stearic acid (C18:0)) increased in the mining area, whereas total unsaturated fatty acids (ΣTUSFA; oleic acid (C18:1), linoleic acid (C18:2), and α-linolenic acid (C18:3)) were higher under non-mining conditions. From a palynological perspective, the increased metal load preserved morphological integrity in the pollen of H. scabrum, whereas it caused pronounced changes in the P/E ratio and pollen shape in H. lydium, with statistically significant differences observed. Overall, the findings suggest that mining-related heavy metal stress influences metal accumulation, fatty acid composition, and pollen characteristics in Hypericum species, although the magnitude and nature of these effects differ between H. scabrum and H. lydium. These species-specific differences indicate that the two species exhibit distinct physiological and morphological responses to heavy metal stress, contributing to a better understanding of plant-heavy metal interactions in mining ecosystems.

PMID 42723791
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PubMedCureus2026-09-11

Efficacy of Sublingual Misoprostol Versus Intravenous Tranexamic Acid in Reducing Blood Loss Among Full-Term Pregnant Women Undergoing Primary Lower Segment Caesarean Section: A Randomized Controlled Trial.

Basavaraj Nikhitha N, B Ashwini A, Pushpa Kotur K

Postpartum hemorrhage remains a major cause of maternal morbidity and mortality, with caesarean section being associated with increased intraoperative blood loss. Pharmacological agents such as misoprostol and tranexamic acid have been used prophylactically to reduce blood loss during lower segment caesarean section (LSCS); however, evidence directly comparing their efficacy is limited. This study aimed to compare the efficacy and safety of sublingual misoprostol and intravenous tranexamic acid in reducing intraoperative blood loss during primary LSCS. This hospital-based, open-label, randomized controlled trial included 140 women with singleton term pregnancies undergoing primary LSCS. Participants were randomized equally to receive either 600 µg sublingual misoprostol or 1 g intravenous tranexamic acid immediately before skin incision. The primary outcome was intraoperative blood loss measured using a standardized gravimetric method. Secondary outcomes included postoperative fall in haemoglobin, requirement for additional uterotonic agents or blood transfusion, and adverse drug effects. Baseline demographic and obstetric characteristics were comparable between the two groups. Mean intraoperative blood loss was significantly lower in the misoprostol group than in the tranexamic acid group (316.0 ± 158.0 mL vs. 518.5 ± 233.1 mL; p < 0.001). Women receiving misoprostol also had a significantly smaller postoperative fall in haemoglobin and required fewer additional uterotonic agents (2 (2.9%) vs. 11 (15.7%); p = 0.009) and blood transfusions (1 (1.4%) vs. 9 (12.9%); p = 0.016). Fever and shivering were more common with misoprostol, whereas hypotension occurred more frequently in the tranexamic acid group (all p < 0.05). Sublingual 600 µg misoprostol was more effective than 1 g intravenous tranexamic acid in reducing intraoperative blood loss during primary LSCS. It was associated with a smaller postoperative decline in haemoglobin and a reduced need for additional uterotonic agents and blood transfusion, while maintaining an acceptable safety profile. These findings support the use of sublingual misoprostol as an effective and economical option for preventing excessive blood loss during primary LSCS.

PMID 42724954
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PubMedJournal of microbiology and biotechnology2026-09-11

Local Suppression of Dgat2 Augments Fatty Acid Oxidation in Skeletal Muscle in High-Fat Diet-Fed Mice.

Jiyun Yeo Y, Park Ju Young JY, Kwon Min Gyeong MG, Kim Eun Seong ES et al.

Diacylglycerol acyltransferase 2 (DGAT2) codes an enzyme which synthesize triglyceride by esterifying fatty acid to last portion of diacylglycerol backbone, and contributes to intramyocellular lipid metabolism. Small interfering RNA (siRNA)-mediated knockdown of Dgat2 was previously shown to reduce AKT phosphorylation and glucose uptake, decrease fatty acid partitioning into triglycerides, and increase free fatty acid release and oxidation in skeletal muscle cells. The current study aimed to determine whether Dgat2 knockdown affects lipid and glucose metabolism in glycolytic muscle (GM) and oxidative muscle (OM) under high-fat diet conditions, consistent with our previous in vitro findings. Male C57BL/6J mice were fed high-fat diet, and treated with Dgat2 or control-siRNA, and the effects were compared in different muscle types. Muscle Dgat2 suppression reduced intramuscular triglyceride content by up to 38.2% whereas increased circulating triglyceride levels. In addition, decreased Gpat3 mRNA levels supported a reduction in lipid esterification capacity. Dgat2 suppression increased the integration of C14-tagged fatty acids into acid-soluble metabolites, and altered gene expressions related to glucose utilization; GLUT4 protein were decreased and Pdk2 mRNA increased in both GM and OM fibers. GM exhibited decreased AKT phosphorylation about 50%, whereas OM showed no change in AKT phosphorylation. Noticeably OM exhibited reduced Hk2 and glycogen accumulation. Together, these findings suggest that muscle Dgat2 inhibition redirects fatty acid channeling from triglyceride storage toward oxidation in vivo, with accompanying changes in glucose metabolism-related markers. These results extend our previous cell-based findings to a more physiologically relevant setting, while highlighting distinct response patterns in GM and OM.

PMID 42723533
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PubMedNature communications2026-09-11

Electrochemical hydrogenation of biomass substrates with cation shuttling in a solid electrolyte reactor.

Zhai Yanjie Y, Gong Shanhe S, Zuo Yunpeng Y, Sun Libo L et al.

Electrochemical hydrogenation of biomass-derived substrates offers a sustainable route to valuable chemicals, yet conventional systems often struggle to simultaneously achieve high efficiency and high product purity. Here we report an electrochemical process based on a porous solid-electrolyte reactor that integrates efficient hydrogenation with intrinsic purification for biomass-derived substrates, thereby eliminating the need for supporting electrolytes. The system promotes the hydrogenation of maleic acid solution (a model unsaturated biomass substrate) into succinic acid (a model saturated biomass substrate), via a cation shielding effect while suppressing competing reactions such as hydrogen evolution. By continuously recycling the generated sodium succinate from the cathode to the middle layer, the reactor further converts it into pure succinic acid, establishing a closed-loop alkali-metal-cation shuttle that enhances selectivity and minimizes side reactions. This system delivers succinic acid Faradaic efficiencies ~ 85%, long-term operational stability (over 500 hours), and a final solution of > 98% purity, without downstream electrolyte recovery. These results highlight a scalable pathway toward cleaner, more efficient electrochemical upgrading of biomass.

PMID 42722657
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PubMedTranslational pediatrics2026-09-11

Metabolic reprogramming rewires aberrant immune responses to drive endothelial dysfunction in Kawasaki disease: a narrative review.

Zhao Zixuan Z, Wang Shuhui S, Li Xuan X, Zhu Liyan L et al.

Kawasaki disease (KD) is a systemic pediatric vasculitis characterized by dysregulated immune activation and substantial risk of coronary artery lesions. Emerging evidence suggests metabolic reprogramming is a critical link between immune responses and endothelial dysfunction during KD progression. This review aims to provide an integrated overview of metabolic alterations in KD pathogenesis, focusing on clinical observations, mechanistic insights, and experimental evidence. A literature search was conducted using PubMed and Web of Science to identify studies published up to July 2026, combining "Kawasaki disease" with terms related to metabolism and metabolic pathways, including metabolites, glucose, glycolysis, amino acids, lipids, fatty acid oxidation, succinic acid, the tricarboxylic acid (TCA) cycle, nitric oxide, urine, gut microbiota, mouse models, and therapeutic strategies. Relevant clinical, experimental, and mechanistic studies were reviewed and synthesized. Accumulating evidence indicates extensive metabolic remodeling in KD, including enhanced glycolysis, disrupted lipid metabolism and fatty acid oxidation, altered amino acid metabolism, and TCA cycle perturbations. These abnormalities are closely linked to immune activation, mitochondrial dysfunction, oxidative stress, and vascular inflammation. KD mouse models further support metabolic reprogramming, marked by altered tryptophan and amino acid metabolism, lipid metabolism, and lactate production. Notably, kynurenine pathway activation with reduced tryptophan availability is associated with inflammatory amplification and mitochondrial impairment. Beyond host-derived changes, gut microbiota dysbiosis and its metabolites appear to correlate with immune responses and disease severity. However, clinical translation of these metabolic signatures into reliable biomarkers or therapeutic targets remains limited. This review highlights metabolic reprogramming as a key interface linking immune dysregulation, endothelial injury, and vascular complications in KD. Metabolic abnormalities may act not merely as consequences of inflammation but as active regulators of vascular dysfunction and disease progression. Significant gaps remain in establishing causal relationships between specific metabolic alterations and KD pathogenesis. Future studies integrating multicenter cohorts with cellular, multi-omics, and animal model approaches, particularly centered on the metabolic-immune-vascular injury axis, will be essential for identifying novel biomarkers and therapeutic strategies.

PMID 42724070
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