Chinese Herbal Medicines
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2026
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IF 11.2
Fanghong Li,Xiaojiaoyang Li,Yajie Cai,Yufei Li,Yang Yang,Jianan Li,Ruiyu Wu,Ranyi Luo,Rong Sun,Runping Liu
Objective To investigate the therapeutic effects of Sini San (SNS) in cholestatic mice, and to elucidate underlying mechanisms and bioactive ingredients. Methods Through a metabolomics approach, this study identified bioactive components in SNS that were absorbed into the bloodstream. Transcriptomics were performed to identify intrahepatic targets of SNS. Results These findings demonstrated that SNS significantly attenuated partial bile duct ligation (pBDL)-induced cholestatic liver injury by activating intrahepatic (peroxisome proliferator-activated receptor alpha, PPAR α ). SNS-mediated PPAR α activation significantly modulated the expression of bile acid transporters to facilitate intrahepatic bile acid homeostasis and simultaneously ameliorates hepatic inflammation. This study identified marmin, astilbin, poncirin, and isosinensetin as potential PPAR α agonists among absorbed SNS components. Subsequently, PPAR α inhibitor (GW6471), significantly abolished the regulative effects of SNS on lipid and bile acid metabolism. Conclusion This research not only underscores the regulative role of PPAR α in bile acid metabolism but also indicates the presence of potential PPAR α agonists in SNS, offering a novel therapeutic strategy for treating cholestatic liver disease.
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高影响因子
Current Research in Food Science
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2024
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IF 6.2
Weidong Xu,Shasha Tian,Guanqun Mao,Yu Li,Hua Qian,Wenhua Tao
Sini San (SNS) is used to treat liver depression and is applied in both food and herbal medicine. Hyperprolactinemia (HPRL) is a common endocrine disorder, and patients with HPRL are usually associated with depressive symptoms. However, whether SNS is effective in treating HPRL combined with liver depression and its underlying mechanisms are unknown. We applied network pharmacology and molecular docking to predict the mechanism of SNS for the treatment of liver-depressed HPRL. Therapeutic effects were validated in animal models and cells. Metabolomics was also used to evaluate the effect of SNS on liver-depressed HPRL. Network pharmacology and molecular docking analysis showed that AKT1, TNF and IL6 were the key targets, and SNS improved depressive behaviors, regulated sex hormone levels, and improved ovarian morphology. Combined network pharmacology and metabolomics analyses showed that SNS could act by regulating lipid metabolism. In addition, SNS significantly reduced the release of prolactin (PRL) in rat pituitary tumor MMQ cells. Overall, SNS can significantly treat HPRL liver depression at both animal and cellular levels, and effectively alleviate the related symptoms by regulating lipid metabolism. AKT1, TNF and IL6 may be key targets.
研究领域:
药理学
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内分泌学
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神经科学
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分子生物学
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高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 5.4
Xiang-Ling Qin,Hu-Dong Lv,Qi Yang,Bi-Xia Jin,Jing Ge,Ke-Xuan Wu,Jie-Ge Huo,Nan Yao,Song-Lin Li,He Zhu,Jing Zhou
Ethnopharmacological relevance In traditional Chinese medicine (TCM), oxaliplatin-induced peripheral neuropathy (OIPN) is understood as a manifestation of “blood impediment” and “flaccidity” syndromes caused by blood deficiency and cold stagnation in the meridians. Danggui Sini Decoction (a well-known warming formula composed of seven herbs: Danggui, Guizhi, Baishao, Xixin, Gancao, Tongcao, and Dazao) is specifically indicated for these patterns. It works by nourishing blood and warming the meridians, and has been used clinically to alleviate OIPN. However, modern processing methods such as ethanol precipitation may remove insoluble components (e.g., polysaccharides), raising concerns regarding potential efficacy loss. Aim of the study To investigate the impact of removing the ethanol-precipitated fraction on the neuroprotective effects and mechanisms of Danggui Sini Decoction. Materials and methods The Danggui Sini Decoction extract (DSD) was fractionated via ethanol precipitation into precipitate (PAP) and supernatant (SAP), followed by compositional characterization. OIPN was induced in mice, which were then treated with DSD, PAP, or SAP. Neurotoxicity was assessed by behavioral tests, histopathology (H&E and Nissl staining) of the sciatic nerve and dorsal root ganglia (DRG), and serum levels of NT/NGF (ELISA). The gut barrier (H&E; IHC for ZO-1/occludin), abundance of Prevotellaceae_UCG-001 (qPCR), short-chain fatty acids (SCFA) levels (LC-MS), and glutathione (GSH) cycle metabolites (ELISA, LC-MS) were analyzed respectively. Cdk5/p35 pathway was evaluated both in vitro (ND7/23 cells) and in vivo by qRT-PCR and IHC. Results PAP contained 90.1 % saccharides, including polysaccharides (85.5–1494.7 kDa) and a low-molecular-weight saccharide (237.0 Da). All treatments ameliorated OIPN: DSD > SAP > PAP in pain relief and nerve protection; DSD > PAP > SAP in NGF/NT restoration. All improved colonic structure (DSD > PAP > SAP) and Prevotellaceae_UCG-001 (PAP > DSD > SAP). DSD has the most ability to increase butyrate, acetate, and propionate, followed by PAP, and the worst is SAP. In addition, SAP has the most significant effect on reversing GSH depletion. In vitro, sodium butyrate (NaB), DSD, SAP, and PAP downregulated the expression of calmodulin , Camk2a , Cdk 5 , and Cdk5r1 . In vivo, all reduced DRG CaMKII, Cdk 5, and p35, though PAP and SAP were less than DSD. Conclusion PAP, the ethanol-precipitated saccharide fraction, is essential for DSD in the treatment of OIPN. PAP particularly regulated gut microbiota (e.g., Prevotellaceae_UCG-001 ) and enhanced SCFAs production (especially butyrate), indirectly suppressing Cdk5/p35 pathway via the potential GSH cycle; SAP primarily prevented GSH depletion, an effect that may be associated with direct modulation of the GSH cycle. PAP and SAP synergistically contribute to DSD on the treatment of OIPN through complementary pathways.
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CELL BIOCHEMISTRY AND BIOPHYSICS
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2014
·Vol. 71
·期 2
·945-950
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IF 2.38
Chen Qing-quan,Han Xuesong,Wang Wan-ming,Zhao Liangyu,Chen Aimin
Danggui Sini decoction (DSD), a famous Chinese medicine, has been used therapeutically in various diseases. In this study, we tried to investigate whether and how DSD could ameliorate myelosuppression in an animal model, in which myelosuppression is induced by cyclophosphamide treatment. The myelosuppression model was established by intraperitoneal injection of 100 mg/kg cyclophosphamide in mice. Flow cytometry was used to assess cell numbers and evaluate the bone marrow cell cycle distribution. Spleen samples were collected, and the mRNA expression levels of thrombopoietin (TPO) and c - Mpl were analyzed by RT-PCR. Our results demonstrated that DSD could significantly elevate the level of bone marrow hematopoietic stem progenitor cells in myelosuppression mice model. DSD also accelerated cell proliferation by switching cell cycles from G0/G1 phase to S and G2/M phase. Moreover, DSD significantly elevated the mRNA expression level of TPO , but not c - Mpl in spleen. Overall, the present results indicated that DSD is a promising Chinese medicine that is highly potent to ameliorate myelosuppression induced by chemotherapy by upregulating TPO expression.
研究领域:
药理学
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血液学
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肿瘤学
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分子生物学
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Chinese Herbal Medicines
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2024
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IF 4.7
Cuiping Long,Qian Zhou,Min Xu,Xin Ding,Xingxing Zhang,Ya Zhang,Yuping Tang,Guangguo Tan
Objective Myocardial inflammation during myocardial infarction (MI) could be inhibited by regulating arachidonic acid (AA) metabolism. Recent studies demonstrated that Sini Decoction (SND) was identified to be an effective prescription for treating heart failure (HF) caused by MI. But the anti-inflammatory mechanism of SND remained unclear. The work was designed to investigate the anti-inflammatory mechanism of SND through the AA metabolism pathway in vitro and in vivo experiments. Methods An inflammatory injury model of H9c2 cells was established by lipopolysaccharide (LPS)-stimulated macrophage-conditioned media (CM). The animal MI model was built by the ligation of left anterior descending (LAD) branch of coronary artery in rat. Meanwhile, the rats were divided into five groups: sham group, MI group, MI + Celecoxib group, MI + low-dose SND group (SND-L) and MI + high-dose SND group (SND-H). Cardiac function, histopathological changes and serum cytokines were examined four weeks later. Western blot analysis was conducted to verify the key enzymes levels in the AA metabolic pathway, including phospholipase A2 (PLA2), cyclooxygenases (COXs) and lipoxygenases (LOXs). Results These in vivo results demonstrated that SND could improve the cardiac function and pathological changes of rats with MI, and regulate the key inflammatory molecules in the AA metabolism pathway, including sPLA2, COX-1, COX-2, 5-LOX and 15-LOX. In vitro , SND could decrease the release of pro-inflammatory cytokines including TNF-α and IL-6 and inhibit cell apoptosis in CM-induced H9c2 cells. Moreover, SND could protect H9c2 cells from the damage of CM by regulating nuclear factor kappa-B (NF-κB) signal pathway and the expression of COX-2. Conclusion SND may be a drug candidate for anti-inflammatory treatment during MI by regulating the multiple targets in the AA metabolism pathway.
研究领域:
药理学
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心脏病学
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分子生物学
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炎症研究
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高影响因子
PHYTOMEDICINE
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2024
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IF 6.7
Zhang Di,Chen Zhenni,Zhuang Zifeng,Jing Bei,Cao Yong,Li Yixuan,Pan Yuwei,Gao Li,Chen Jiaxu,Zhao Guoping
Ethnopharmacological relevance Danggui Sini Decoction (DGSD), which is commonly used to treat sciatica, has been shown to have an analgesic effect, but the underlying mechanisms are unclear. Here, Danggui Sini Decoction was shown to normalize the intestinal microbiota and serum metabolite levels to exert an analgesic effect. Aim of the study This study aimed to elucidate the therapeutic effects of DGSD on sciatica and the underlying mechanisms involved. Methods In this study, we conducted chronic constriction injury (CCI) model. Mecobalamin and DGSD were administered to CCI rats. Behavioural tests were used to examine the therapeutic effects of the drugs. UHPLC was used to identify DGSD components. 16S rRNA gene sequencing analysis of the intestinal flora was used to analyse the effect of DGSD on the intestinal microbiota. UHPLC‒MS/MS was used to identify blood metabolites. KEGG pathway analysis of differentially abundant metabolites was subsequently conducted. ELISA was used to measure the serum inflammatory factor levels, and correlation analysis between the serum inflammatory factor levels and intestinal microbe abundance was conducted. PCR, western blotting, and immunohistochemical staining were used to validate the results of the KEGG pathway analysis. Results After CCI, the rats exhibited obvious thermal hyperalgesia; disruption of sciatic nerve structure; increased IL1α, SP, CCL5, and PGE2 levels; decreased IL10 levels in the blood; increased IL1β, IL6, COX2, MMP9, nNOS, and p-NF-κB levels; and decreased IL4 levels in the sciatic nerve. In addition, CCI led to increased abundances of Peptostreptococcaceae, Leuconostocaceae, Christensenellaceae, Akkermansiaceae, Staphylococcaceae, Romboutsia, Marvinbryantia, Turicibacter, Weissella, UCG-005, Christensenellaceae_R-7_group, Akkermansia, Staphylococcus, Romboutsia_ilealis, Weissella_paramesenteroides, and Akkermansia_muciniphila and decreased abundances of Lactobacillaceae, Lactobacillus, Lactobacillus_murinus, and Lactobacillus_johnsonii. Correlation analysis indicated that Turicibacter abundance was most strongly related to IL1α, PGE2, IL10, and CCL5 levels, while norank_o_Coriobacteriales abundance had the weakest relationship with SP levels. KEGG pathway analysis of the differentially abundant metabolites revealed that the ‘NF-kappa B signalling pathway’ was involved in sciatica. DGSD reduced the levels of inflammatory factors, including IL1α, SP, CCL5, PGE2, IL6, COX2, and MMP9, in the blood and sciatic nerve and inhibited nNOS and NF-κB phosphorylation. DGSD improved the abundance of probiotics, including Lactobacillus and Blautia, and lowered the abundance of harmful bacteria, including Romboutsia, Turicibacter, and Weissella. DGSD promoted the repair of the injured sciatic nerve. Conclusions DGSD can treat sciatica by inhibiting intestinal microbiota disorders induced by CCI in rats, normalizing inflammatory factor levels, and promoting nerve repair.
研究领域:
药理学
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神经科学
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微生物学
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代谢组学
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民族药理学
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高影响因子
BIOTECHNOLOGY LETTERS
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2021
·Vol. 43
·期 3
·677-690
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IF 2.461
Zhang Chaolei,Wang Chao,Zhao Shan,Xiu Zhilong
Objectives Probiotics ( Bacillus subtilis 04178) were entrapped in alginate-chitosan microcapsules by high-voltage electrostatic process. The encapsulation pattern was established as entrapped low density cells with culture (ELDC wc ). The performance of ELDC wc cells was investigated against stress environments of simulated digestive fluids. Results After incubation in simulated gastric (pH 2.5) and intestinal fluids (4% bile salt) for 2 h, the survival rate of ELDC wc cells (18.19% and 27.54%) was significantly higher than that of the free cells (0.0000009% and 0.0005%). The reason why B. subtilis embedded in microcapsules can resist the stress environments was that the mass production of extracellular proteins and polysaccharides prompted B. subtilis to form cell aggregates. The production of extracellular proteins and polysaccharides were regulated by the concentration of c-di-GMP and the expression of ydaJKLMN operon, abbA , sinI , slrA , slrB , abrR and sinR . Conclusions c-di-GMP is important for the production of extracellular polymer substance to enhance probiotic viability in stress environments.
研究领域:
微生物学
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生物技术
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食品科学
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PubMed
高影响因子
Frontiers in Cardiovascular Medicine
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2026
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IF 3
Haipeng Tang,Zhiliang Sun,Shanshan Wang,Zhi Chen,Wenzhu Wang,Yang Wang,Jiyu Gong,Xiaoyan Xie,Wenyi Gao
BackgroundCoronary heart disease (CHD) remains a major global health burden, and residual cardiovascular risk persists despite guideline-based therapies. Danggui Sini Granule (DSG), a granule formulation derived from the classical Danggui Sini Decoction, has been widely used clinically to improve cardiovascular circulation and alleviate ischemic symptoms; however, its gut-heart-axis-related mechanisms remain insufficiently defined.MethodsA rat model of vasospastic CHD was established using a high-fat diet combined with acute environmental stress and pituitrin injection, followed by treatment with DSG at different doses. Pharmacodynamic effects were evaluated by electrocardiography, histopathology, serum lipids, and inflammatory markers. Gut microbial alterations were profiled using 16S rRNA sequencing. Serum metabolic changes were characterized by untargeted metabolomics. Network pharmacology and joint pathway enrichment were further used to cross-validate target prediction with metabolite-level readouts and to prioritize gut–microbiota–metabolism–phenotype links.ResultsDSG attenuated ST-segment elevation, reduced myocardial histopathological injury, mitigated dyslipidemia, and lowered systemic inflammatory mediators, including TNF-α and IL-6. 16S rRNA analysis showed bidirectional microbiota modulation, with reduced opportunistic/pathogenic genera (e.g., Escherichia, Staphylococcus) and enrichment of potentially beneficial taxa (e.g., Lactobacillus, Clostridium). Metabolomics revealed partial mitigation of CHD-related disturbances, mainly in linoleic acid and arachidonic acid pathways, with restoration of levels of protective lipid mediators including 12,13-DHOME, 3-HIA, and PGE1. Joint pathway analysis integrating reversed metabolites with predicted targets consistently prioritized Lipid and atherosclerosis, PPAR-related metabolic regulation, PI3K-Akt/eNOS-associated vascular protection, and inflammation-related signaling (JAK-STAT and TNF/NF-κB). Furthermore, molecular docking suggested favorable binding affinities between the key components/metabolites (e.g., Quercetin, 12,13-DHOME, PGE1) and core targets within these pathways (including PIK3CA, NOS3, PPARG, TNF, and RELA).ConclusionDSG demonstrated significant cardioprotective effects in vasospastic CHD rats, which were associated with coordinated gut microbiota remodeling, lipid-metabolic reprogramming, and modulation of inflammation-related pathways. These findings, further suggested by in silico molecular docking, provide a multidimensional framework for understanding the cardioprotective potential of DSG from a gut-heart-axis perspective. Given the associative nature of the current multi-omics data, key causal links should be validated in future targeted intervention studies.
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Chinese Medicine
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2025
·Vol. 20
·期 1
·1-21
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IF 5.7
Zhu Fangsi,Ding Yijie,Chen Luyun,Fang Rou,Huang Chengfeng,Liu En,Wang Yingrui,Su Yong,Ge Chaoliang
Background Sini-San (SNS), a classical traditional Chinese medicinal formula, has demonstrated promising potential in mitigating the progression of liver fibrosis (LF). Increasing evidence highlights that disruption of bile acids (BAs) homeostasis is critically involved in the pathogenesis and progression of LF, suggesting that targeting BAs metabolism could represent a therapeutic strategy. This study aimed to explore whether the protective effects of SNS against LF are mediated through modulation of BAs metabolism and associated regulatory pathways. Methods The chemical constituents of SNS were characterized using high-performance liquid chromatography (HPLC). LF models were established in mice through intraperitoneal injection of carbon tetrachloride (CCl 4 ) or feeding a high-fat, high-sugar (HFHS) diet. SNS was administered orally. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hydroxyproline (HYP) levels were measured, and liver histopathology was evaluated by hematoxylin–eosin (HE), Masson and TUNEL staining. The expression of fibrosis- and apoptosis-associated markers (Collagen-1, α-SMA, Bcl-2, Bax, and Caspase-3) was assessed by RT-qPCR and Western blotting. Serum BAs profiles were analyzed using LC–MS/MS, and molecules involved in BA metabolism (Fxr, Cyp7a1, Cyp27a1, Bsep, Ntcp, Asbt and OATP) were examined. Gut microbiota composition was analyzed through 16S rRNA gene sequencing. To investigate the mechanisms by which SNS regulates BAs homeostasis, additional experiments were conducted under choline chelation, pseudo-sterile conditions, and in fxr −/− mice. Results In LF mice induced by CCl 4 or HFHS diet, significant alterations were observed in BAs levels and composition. The expression of BAs-synthesizing enzymes (CYP7A1, CYP27A1), BAs transporters ( Bsep, Ntcp, Asbt and Oatp ), and the feedback regulatory receptor FXR was markedly dysregulated. Meanwhile, gut microbiota abundance and composition were also significantly disrupted, indicating a disturbance of BAs homeostasis. SNS treatment effectively alleviated liver injury and fibrosis, corrected BAs imbalance, regulated the expression of BAs-related genes, and restored microbial diversity. However, the antifibrotic effects of SNS were reversed by choline chelation, antibiotic treatment, and fxr knockout. Conclusions SNS may exert anti-hepatic fibrosis effects by modulating BAs metabolism and gut-liver axis pathways, ultimately restoring BAs homeostasis. These findings provide new insights into the therapeutic mechanisms of SNS and suggest its potential as a multitargeted strategy for LF treatment.
研究领域:
药理学
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中医中药
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肝脏病学
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代谢学
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微生物组研究
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高影响因子
BMC Complementary Medicine and Therapies
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2025
·Vol. 26
·期 1
·9
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IF 3.4
Zhu Liangting,Hu Junjie,Li Juan,Qu Xinyue,Zhou Xian,Gan Guoping,Liu Yanwen,Liu Songlin,Chen Xin
Background Sini San (SNS) is a traditional Chinese medicinal formulation originating from the “ Treatise on Febrile Diseases ”, an ancient text that has been historically employed for treating depression. However, the underlying mechanisms by which SNS potentially ameliorates symptoms of depression remain unclear. This study aimed to elucidate the role of gut microbiota in tryptophan metabolism and examine the involvement of short-chain fatty acids (SCFAs) in the putative antidepressant effects of SNS. Methods A rat model of depression using chronic unpredictable mild stress (CUMS) was established through simultaneous modeling and treatment for six consecutive weeks. The possible therapeutic effect of SNS on CUMS-induced rats was thoroughly assessed using body weight measurements, open-field tests, and sucrose preference tests. Alterations in rat gut microbiota were analyzed using full-length 16 S rRNA third-generation sequencing. Furthermore, metabolomic analysis was performed on fecal samples. An enzyme-linked immunosorbent assay (ELISA) was used to quantify tryptophan (Trp), serotonin (5-HT), and kynurenine (Kyn) in the hippocampal and colonic tissues. Reverse transcription quantitative PCR (RT-qPCR) was used to measure the mRNA levels of TPH-1 and TPH-2 in hippocampal and colonic tissues. Immunofluorescence was used to assess hippocampal IDO-1 and IBA-1 expression. Finally, gas chromatography-mass spectrometry (GC-MS) was used to analyze the SCFAs content in fecal samples. Results Administration of SNS significantly alleviated depressive symptoms induced by CUMS, as demonstrated by increased body weight, improved sucrose preference, and a statistically significant decrease in immobility time during the forced swim test ( P < 0.05). The Shannon and Simpson indices were elevated following SNS treatment, signifying an enhancement in both the quantity and variety of the gut microbiota. Analysis using 16 S rRNA gene sequencing revealed that SNS influenced the composition of the gut microbiome, favorably increasing the presence of beneficial bacteria, such as Firmicutes , Lactobacillaceae , Ruminococcaceae , and Oscillospiraceae , while simultaneously decreasing the levels of potentially detrimental bacteria, such as Muribaculaceae , Prevotellaceae , Lachnospiraceae , and Alloprevotella . Fecal metabolomic studies identified 87 metabolites, of which 57 were differentially expressed, most notably l-tryptophan and phenylalanine. These metabolites were primarily linked to 15 metabolic pathways, with notable enrichment in the biosynthetic pathways of phenylalanine, tyrosine, and tryptophan, as well as the metabolic pathways of arachidonic acid and phenylalanine. Metabolomic profiling indicated that SNS stimulated the kynurenine pathway, leading to increased levels of metabolites with antidepressant properties, such as Trp, 5-HT, and Kyn, in both hippocampal and colonic tissues. In addition, SNS promoted the synthesis of SCFAs, particularly butyrate and propionate, which are known for their neuroprotective properties. Conclusions The present study suggests that the antidepressant effects of SNS can be attributed to its ability to modulate the structure of the gut microbiota, consequently regulating tryptophan metabolism and SCFA levels, which ultimately ameliorate symptoms of depression. These findings provide experimental evidence supporting the concept of the brain-gut axis in depression treatment and lay a foundation for further investigation of the underlying antidepressant mechanisms of the SNS.
研究领域:
药理学
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神经科学
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微生物组研究
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中医中药
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代谢组学
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高影响因子
PHYTOMEDICINE
·
2024
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IF 6.7
Junling Ren,Xia Wang,Yuran Sun,Le Yang,Hui Sun,Ye Sun,Ling Kong,Guangli Yan,Ying Han,Xijun Wang
Background Danggui Sini Decoction (DGSND) is a classic prescription for treating primary dysmenorrhea (PD), while, the ameliorating effects of DGSND on PD and its mechanisms are not yet fully understood. Purpose The present study is devoted to investigate the protective effect of DGSND against PD and the possible mechanism from the perspective of metabolomics as well as lipidomics. Methods DGSND was characterized by UPLC-Q-TOF/MS. The PD rat model was induced by estradiol benzoate and oxytocin, and traditional pharmacology, including writhing times, latency time, biochemical index, organ index, and histopathology were performed to evaluated the efficacy of DGSND on PD. Urine metabolomics strategy combined with functional analysis was adopted to delineate the therapeutic effect of DGSND on PD rats and anchor the crucial pathway, and lipidomics analysis was further performed with the uterine tissue as the research object to elucidate the protective mechanism of DGSND from the perspective of lipid homeostasis. Finally, western blot analysis was used to validate the expression of key metabolic enzymes in lipid metabolism. Results DGSND was effective in ameliorating writhing times, latency time, the value of prostaglandin F 2α (PGF 2α )/PGE 2 , uterus index, and morphological changes of PD rats. Metabolic signature of PD rats was primarily characterized by the disturbance of steroid hormone metabolism, amino acid metabolism, and lipid metabolism. Functional analysis revealed the urine biomarkers of PD were most related with lipid abnormality. Further lipidomics analysis indicated DGSND exerted anti-PD effects by remodeling lipid homeostasis, which might be due to the significant correlations between different kinds of lipids, especially the extremely high correlation of phosphatidylethanolamine, phosphatidylcholine, and fatty acids. Moreover, the key metabolic enzymes expression of CK, PLA 2 , LPCAT3, COX-2, and 5-LOX can be greatly downregulated by DGSND. Conclusion Our findings demonstrated a novel protective mechanism of DGSND against PD by regulating lipid homeostasis.
研究领域:
药理学
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代谢组学
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脂质组学
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中医
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动物模型
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高影响因子
Chinese Journal of Integrative Medicine
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2026
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IF 3.1
Zhang Di,Zhuang Zi-feng,Lin Shao-zi,Chen Zen-ni,Chen Hong-ling,Gu Jun-yan,Hao Yu-ting,Li Yi-xuan,Chen Jia-xu,Zhao Guo-ping
Objective To elucidate whether Danggui Sini Decoction (DGSD) relieves sciatica by downregulating transient receptor potential (TRP) channels involved in peripheral sensitization. Methods After conducting chronic constriction injury of sciatic nerve (CCI) operation, 32 SD rats, randomly assigned to the sham, CCI 7d, CCI 14d, and CCI 21d groups ( n =8 per group), were used to observe the course of sciatica. mRNA sequencing of dorsal root ganglia (DRG) was conducted on rats in the sham and CCI 21d groups. Another 32 rats were divided into the sham, CCI, mecobalamin, and DGSD groups, 8 in each group. mRNA sequencing analysis and single-cell RNA-sequencing (scRNA-seq) data analysis were conducted. Behavioural tests were conducted to evaluate the therapeutic effects of DGSD. The levels of TRP vanilloid (TRPV)1–4, TRP ankyrin 1 (TRPA1), TRP melastatin 8 (TRPM8), Ras homolog family member A (RhoA), and phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) were measured via Western blot, and the serum levels of C-C motif chemokine ligand 2 and 5 (CCL2, CCL5), substance P (SP), and prostaglandin E2 (PGE2) were conducted via ELISA. Results scRNA-seq and mRNA sequencing analysis revealed that inflammatory mediator regulation of TRP channels played a role in the development of sciatica. CCI rats exhibited cold hyperalgesia from day 4 to 21, increased the DRG protein expression levels of TRP channels, including TRPV1–4, TRPA1, TRPM8, RhoA, p-p38MAPK, CCL2, CCL5, SP, and PGE2. Treatment with DGSD decreased the serum levels of CCL2, CCL5, SP, and PGE2, and reduced the levels of RhoA, p-p38MAPK, TRPV1–4, TRPA1, and TRPM8 in DRG ( P <0.05). Conclusion CCI increased the levels of TRP channels and inflammatory factors, inducing cold hyperalgesia, whereas DGSD relieved pain via inhibiting peripheral sensitization to relieve cold hyperalgesia by reducing the inflammatory factors and TRP.
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