Olfactory receptors (ORs) form the largest superfamily of G protein-coupled receptors (GPCRs). Traditionally recognized for their role in the nasal olfactory epithelium, where they mediate the sense of smell, accumulating evidence has firmly established their ectopic expression in non-olfactory tissues, including the intestine, lungs, and kidneys. The intestine, as the primary site for nutrient digestion and absorption, harbors a highly complex chemical environment. To adapt to this environment, the gut employs a sophisticated network of “chemosensors” to monitor luminal contents and maintain homeostasis. Among these sensors, intestinal ORs have emerged as crucial functional components, serving as a molecular bridge that connects environmental chemical signals—such as food-derived odorants—to specific physiological responses. This discovery has significantly deepened our understanding of how dietary flavors and compounds influence intestinal physiology at the molecular level. This review systematically summarizes the expression profiles, ligand classification, and biological functions of ORs within the gastrointestinal tract. Studies indicate that intestinal ORs exhibit distinct spatial distribution patterns across different gut segments and display cell-type specificity, particularly within enterocytes and enteroendocrine cells. These receptors function as versatile sensors capable of recognizing a wide variety of ligands, including exogenous dietary components, gut microbiota metabolites such as short-chain fatty acids, and endogenous small molecules like azelaic acid. Upon activation by specific ligands, intestinal ORs trigger intracellular signaling cascades, primarily involving the AC-cAMP-PKA pathway or calcium influx channels. A major focus of this review is to elucidate the molecular mechanisms by which these receptors regulate the secretion of gut hormones. Activation of specific ORs in enteroendocrine cells has been shown to stimulate the release of hormones such as glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and serotonin (5-HT), thereby modulating systemic energy metabolism, glucose homeostasis, and gastrointestinal motility. Furthermore, the review addresses the critical roles of ORs in immune regulation and pathology. Evidence suggests that specific ORs contribute to the maintenance of intestinal immune homeostasis and may offer protection against inflammation. Beyond their involvement in inflammatory responses, ORs such as Olfr78 have been shown to regulate the differentiation and function of intestinal endocrine cells. Similarly, Olfr544 has been demonstrated to alleviate intestinal inflammation by remodeling the gut microbiome and metabolome. These findings collectively suggest that specific ORs hold promise as therapeutic targets for mitigating intestinal inflammation and maintaining gut homeostasis. Additionally, the review explores the emerging role of ORs in cancer. Although OR expression is often downregulated in tumor tissues compared to normal mucosa, activation of specific ORs by certain ligands can inhibit tumor cell proliferation and migration and induce apoptosis via pathways such as MEK/ERK and p38 MAPK. Conversely, other receptors, such as OR7C1, may serve as biomarkers for cancer-initiating cells. In conclusion, intestinal ORs represent a vital component of the gut’s sensory network. The review also discusses the translational potential of these findings. By elucidating the precise pairing relationships between dietary components and specific ORs, novel therapeutic strategies could be developed. Intestinal ORs may thus emerge as promising targets for nutritional and pharmacological interventions in metabolic diseases, inflammatory bowel diseases, and malignancies.

Aim To investigate the effect of linarin on improving cognitive behavior of APP/PS1 mice,and to explore the therapeutic effect of linarin on A β deposi-tion and neuroinflammation and its correlation.Meth-ods APP/PS1 transgenic mice were randomly divid-ed into the model group,high-dose group,medium-dose group,low-dose group and positive control group.C57BL/6J mice were set as the normal group.Morris water maze was used to evaluate the learning and mem-ory abilities of mice.TUNEL staining was used to de-tect the apoptosis of neurons in the CA1 region of mice.IHC was used to detect the expression levels of Aβ42 and GFAP.Western blot was used to detect the expression levels of BACE1 and PS-1.Results Com-pared with the normal group,mice of the model group showed lower NCP,shorter target quadrant travel,less target quadrant residence time percentage(all P＜0.01),higher apoptosis rate of neurons in the CA1 re-gion(P＜0.01),significantly higher protein expres-sion levels of A β42 and GFAP(all P＜0.01),and significantly higher protein expression levels of BACE1 and PS-1(all P＜0.01).Compared with the model group,the medium-dose group,high-dose group and positive control group showed higher NCP,longer tar-get quadrant travel,more target quadrant residence time percentage(all P＜0.05),lower apoptosis rate of neurons in the CA1 region(P＜0.01),significantly lower protein expression levels of A β42 and GFAP(all P＜0.01),and significantly lower protein expression levels of BACE1 and PS-1(all P＜0.01).Conclu-sions Linarin can inhibit two key enzymes to reduce the decomposition of APP and the generation of A β42,thereby inhibiting the activation of astrocytes,allevia-ting neuroinflammation,improving the core pathologi-cal features of AD,and thus significantly improving learning and memory impairment in APP/PS1 mice.

Objective:To study the relationship between microRNA (miRNA, miR)-675-3p, miR-675-5p, miR-29b-3p, miR-let-7b-3p and fluoride induced articular cartilage injury in rats.Methods:Using the factorial design, thirty 3-week-old specific pathogen free grade male Wistar rats (weighted 125 - 150 g) were selected and randomly divided into a control group, a 25 mg/L fluoride group, and a 50 mg/L fluoride group using a random number table method, with 10 rats in each group. The control group drank distilled water, while the fluoride exposure groups drank distilled water with fluoride ion concentrations of 25 and 50 mg/L, respectively. Five rats were euthanized in each group at 3 and 6 months of feeding, respectively. Visual observation was used to observe the occurrence of dental fluorosis in rats, and fluoride ion selective electrode method was used to detect the fluoride level in blood, urine, and cartilage. Hematoxylin-eosin staining and safranin O-fast green staining were used to observe the pathological changes of articular cartilage, and Mankin score was used to evaluate the grading of cartilage injury. Real-time fluorescence quantitative PCR was used to detect the expression levels of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage.Results:After 3 and 6 months of fluoride exposure, no dental fluorosis was observed in the control group, while rats in the 25 and 50 mg/L fluoride groups showed varying degrees of dental fluorosis. There were statistically significant differences in the levels of blood fluoride (mg/L: 0.11 ± 0.04, 0.57 ± 0.32, 0.29 ± 0.06, 0.07 ± 0.01, 0.31 ± 0.05, 0.38 ± 0.06), urine fluoride (mg/L: 1.81 ± 0.58, 13.18 ± 2.29, 66.11 ± 20.74, 2.35 ± 1.08, 14.79 ± 3.87, 28.32 ± 4.79), and cartilage fluoride (mg/kg: 341.83 ± 44.07, 612.99 ± 174.72, 991.26 ± 227.32, 338.29 ± 72.53, 957.09 ± 195.86, 1 535.53 ± 89.01) among in rats the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group ( F = 7.76, 42.78, 40.54, 23.10, 18.96, 80.81, P < 0.05). In the 50 mg/L fluoride group, there were statistically significant differences in the levels of urine fluoride and cartilage fluoride of rats exposed for different times ( t = 4.45, - 3.80, P < 0.05). The Mankin score grading for cartilage injury showed that at 3 months of fluoride exposure, there were 4, 0, and 0 rats with normal cartilage in the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group, 1, 4, and 1 rats with mild injury, and 0, 1, and 4 rats with moderate injury, respectively. At 6 months of fluoride exposure, there were 4, 0, and 0 rats with normal cartilage in the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group, 1, 3, and 0 rats with mild injury, 0, 1, and 3 rats with moderate injury, and 0, 1, and 2 rats with severe injury, respectively. Real-time fluorescence quantitative PCR results showed that fluoride exposure dose had individual effects on the expression of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage ( F = 8.68, 7.97, 9.34, 10.14, P < 0.05). There was no individual effect of fluoride exposure time on the expression of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage ( F = 0.00, 0.15, 0.63, 0.53, P > 0.05). However, there was no interaction effect between fluoride exposure time and dose on the above-mentioned miRNA ( F = 0.68, 0.05, 0.22, 0.24, P > 0.05). The correlation analysis results showed that miR-675-3p and miR-675-5p in cartilage were negatively correlated with blood fluoride, urine fluoride, and cartilage fluoride ( r = - 0.37, - 0.42, - 0.56, - 0.53, - 0.57, - 0.53, P < 0.05), while miR-29b-3p and miR-let-7b-3p were positively correlated with urine fluoride and cartilage fluoride ( r = 0.58, 0.40, 0.48, 0.47, P < 0.05). The results of ordered logistic regression analysis showed that miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p were influencing factors of dental fluorosis grading ( OR = 0.13, 0.04, 1.55, 2.58, P < 0.05) and Mankin score grading ( OR = 0.04, 0.06, 1.41, 1.58, P < 0.05). Conclusion:MiR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p may be involved in the process of fluoride induced articular cartilage injury.

Objective:To study the relationship between microRNA (miRNA, miR)-675-3p, miR-675-5p, miR-29b-3p, miR-let-7b-3p and fluoride induced articular cartilage injury in rats.Methods:Using the factorial design, thirty 3-week-old specific pathogen free grade male Wistar rats (weighted 125 - 150 g) were selected and randomly divided into a control group, a 25 mg/L fluoride group, and a 50 mg/L fluoride group using a random number table method, with 10 rats in each group. The control group drank distilled water, while the fluoride exposure groups drank distilled water with fluoride ion concentrations of 25 and 50 mg/L, respectively. Five rats were euthanized in each group at 3 and 6 months of feeding, respectively. Visual observation was used to observe the occurrence of dental fluorosis in rats, and fluoride ion selective electrode method was used to detect the fluoride level in blood, urine, and cartilage. Hematoxylin-eosin staining and safranin O-fast green staining were used to observe the pathological changes of articular cartilage, and Mankin score was used to evaluate the grading of cartilage injury. Real-time fluorescence quantitative PCR was used to detect the expression levels of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage.Results:After 3 and 6 months of fluoride exposure, no dental fluorosis was observed in the control group, while rats in the 25 and 50 mg/L fluoride groups showed varying degrees of dental fluorosis. There were statistically significant differences in the levels of blood fluoride (mg/L: 0.11 ± 0.04, 0.57 ± 0.32, 0.29 ± 0.06, 0.07 ± 0.01, 0.31 ± 0.05, 0.38 ± 0.06), urine fluoride (mg/L: 1.81 ± 0.58, 13.18 ± 2.29, 66.11 ± 20.74, 2.35 ± 1.08, 14.79 ± 3.87, 28.32 ± 4.79), and cartilage fluoride (mg/kg: 341.83 ± 44.07, 612.99 ± 174.72, 991.26 ± 227.32, 338.29 ± 72.53, 957.09 ± 195.86, 1 535.53 ± 89.01) among in rats the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group ( F = 7.76, 42.78, 40.54, 23.10, 18.96, 80.81, P < 0.05). In the 50 mg/L fluoride group, there were statistically significant differences in the levels of urine fluoride and cartilage fluoride of rats exposed for different times ( t = 4.45, - 3.80, P < 0.05). The Mankin score grading for cartilage injury showed that at 3 months of fluoride exposure, there were 4, 0, and 0 rats with normal cartilage in the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group, 1, 4, and 1 rats with mild injury, and 0, 1, and 4 rats with moderate injury, respectively. At 6 months of fluoride exposure, there were 4, 0, and 0 rats with normal cartilage in the control group, 25 mg/L fluoride group, and 50 mg/L fluoride group, 1, 3, and 0 rats with mild injury, 0, 1, and 3 rats with moderate injury, and 0, 1, and 2 rats with severe injury, respectively. Real-time fluorescence quantitative PCR results showed that fluoride exposure dose had individual effects on the expression of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage ( F = 8.68, 7.97, 9.34, 10.14, P < 0.05). There was no individual effect of fluoride exposure time on the expression of miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p in cartilage ( F = 0.00, 0.15, 0.63, 0.53, P > 0.05). However, there was no interaction effect between fluoride exposure time and dose on the above-mentioned miRNA ( F = 0.68, 0.05, 0.22, 0.24, P > 0.05). The correlation analysis results showed that miR-675-3p and miR-675-5p in cartilage were negatively correlated with blood fluoride, urine fluoride, and cartilage fluoride ( r = - 0.37, - 0.42, - 0.56, - 0.53, - 0.57, - 0.53, P < 0.05), while miR-29b-3p and miR-let-7b-3p were positively correlated with urine fluoride and cartilage fluoride ( r = 0.58, 0.40, 0.48, 0.47, P < 0.05). The results of ordered logistic regression analysis showed that miR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p were influencing factors of dental fluorosis grading ( OR = 0.13, 0.04, 1.55, 2.58, P < 0.05) and Mankin score grading ( OR = 0.04, 0.06, 1.41, 1.58, P < 0.05). Conclusion:MiR-675-3p, miR-675-5p, miR-29b-3p, and miR-let-7b-3p may be involved in the process of fluoride induced articular cartilage injury.

Aim To investigate the effect of linarin on improving cognitive behavior of APP/PS1 mice,and to explore the therapeutic effect of linarin on A β deposi-tion and neuroinflammation and its correlation.Meth-ods APP/PS1 transgenic mice were randomly divid-ed into the model group,high-dose group,medium-dose group,low-dose group and positive control group.C57BL/6J mice were set as the normal group.Morris water maze was used to evaluate the learning and mem-ory abilities of mice.TUNEL staining was used to de-tect the apoptosis of neurons in the CA1 region of mice.IHC was used to detect the expression levels of Aβ42 and GFAP.Western blot was used to detect the expression levels of BACE1 and PS-1.Results Com-pared with the normal group,mice of the model group showed lower NCP,shorter target quadrant travel,less target quadrant residence time percentage(all P＜0.01),higher apoptosis rate of neurons in the CA1 re-gion(P＜0.01),significantly higher protein expres-sion levels of A β42 and GFAP(all P＜0.01),and significantly higher protein expression levels of BACE1 and PS-1(all P＜0.01).Compared with the model group,the medium-dose group,high-dose group and positive control group showed higher NCP,longer tar-get quadrant travel,more target quadrant residence time percentage(all P＜0.05),lower apoptosis rate of neurons in the CA1 region(P＜0.01),significantly lower protein expression levels of A β42 and GFAP(all P＜0.01),and significantly lower protein expression levels of BACE1 and PS-1(all P＜0.01).Conclu-sions Linarin can inhibit two key enzymes to reduce the decomposition of APP and the generation of A β42,thereby inhibiting the activation of astrocytes,allevia-ting neuroinflammation,improving the core pathologi-cal features of AD,and thus significantly improving learning and memory impairment in APP/PS1 mice.

Objective To investigate the effect of cordyceps sinensis(CS)on the activation of fibroblasts through IL-6 trans-signaling pathway and its specific mechanism in the treatment of renal fibrosis.Methods Renal fibrosis mouse model was established by unilateral ischemia/reperfusion(UIR),and the mice were administered intragastrically CS,soluble glycoprotein 130 Fc(sgp130Fc)or Hyper-IL-6.Masson's trichrome staining was utilized to identify tubulointerstitial fibrosis.PAS staining was utilized to assess the extent of renal injury.Western blot was employed to analyze the expression levels of fibrosis markers[alpha-smooth muscle actin(α-SMA),fibronectin(FN)]and proteins associated with IL-6 trans-signaling pathway[phosphorylated signal transducer and activator of transcription 3(p-STAT3),soluble interleukin-6 receptor(sIL-6R)].The expression and localization of proteins were additionally detected by immunohistochemistry,immunofluorescence and qPCR.The effect of cordyceps sinensis extract cordycepin on IL-6 trans-signaling in fibroblasts was further investigated in vitro.Results The results from in vivo experiments showed that administration of CS during the chronic phase demonstrated a beneficial protective impact on inflammation and fibrosis in the affected kidney,and serum creatinine levels and collagen deposition were decreased.Western blot analysis revealed a decrease in the expression levels of α-SMA,FN,as well as IL-6 trans-signaling pathway protein p-STAT3,sIL-6R in the treatment group.Additionally,the mRNA expression levels of chemokines monocyte chemoattractant protein-1(MCP-1)and C-X-C motif chemokine ligand 12(CXCL12)were also decreased in the CS treatment group.Additionally,Hyper-IL-6 can partially counteract the therapeutic effects of CS.In vitro experiments further demonstrated that cordycepin inhibited the secretion of IL-6 from NRK-52E.Combined treatment of recombinant IL-6 and sIL-6R protein activated NRK-49F,leading to a significant increase in α-SMA,FN,and p-STAT3 expression levels.Cordycepin or sgp130Fc treatment significantly inhibited the proliferation of fibroblasts induced by IL-6 trans-signaling pathway.Conclusion CS can significantly reduce IL-6 secretion by renal tubular epithelial cells and inhibit the activation of IL-6 trans-signaling pathway in fibroblasts,thereby ameliorating renal interstitial fibrosis.

In this report, the protective effect and molecular mechanism of Chaihu Shugan San-containing serum on corticosterone(CORT)-induced mitochondrial damage in pheochromocytoma(PC12) cells was studied based on CORT-induced rat PC12 cell model. The cultured cells were divided into five groups: blank control group, CORT group(400 μmol·L~(-1) CORT), Chaihu Shugan San-containing serum group(400 μmol·L~(-1) CORT + 10% Chaihu Shugan San-containing serum), control serum group(400 μmol·L~(-1) CORT + 10% control serum), and fluoxetine group(400 μmol·L~(-1) CORT + 10% fluoxetine-containing serum). The study was carried out by cell activity detection, mitochondrial morphology observation, membrane potential measurement, energy metabolism analysis, and mitochondrial dynamics-related protein detection. The results showed that CORT treatment significantly reduced the survival rate of PC12 cells, altered mitochondrial morphology, and decreased mitochondrial membrane potential and adenosine triphosphate(ATP) synthetic rate. Both Chaihu Shugan San-and fluoxetine-containing serum significantly increased the survival rate of CORT-treated PC12 cells and the ATP synthetic rate in the mitochondria. Unlike fluoxetine, Chaihu Shugan San-containing serum significantly inhibited the decrease in mitochondrial membrane potential caused by CORT and increased the oxygen consumption rate(OCR) values of both mitochondrial maximum respiration and reserve respiration capacity. Western blot analysis showed that CORT induced upregulated protein expressions of dynamin-related protein 1(Drp1) and peroxisome proliferator-activated receptor gamma co-activator 1α(PGC-1α) in PC12 cells and specific protein expression of optic atrophy protein 1(OPA1), yet it repressed the protein expressions of silent information regulator 1(SIRT1) and mitochondrial fusion protein 1(Mfn1) in PC12 cells. Both Chaihu Shugan San-and fluoxetine-containing serum significantly inhibited the protein expression of Drp1. However, only Chaihu Shugan San-containing serum could significantly inhibit the CORT-induced upregulation protein of PGC-1α. RESULTS:: herein suggest that Chaihu Shugan San-containing serum can alleviate CORT-induced damage in PC12 cells, which may be related to the mitochondrial fragmentation/lipid peroxidation protection by Drp1 inhibition, as well as mitochondrial dynamics and energy metabolism mediated by PGC-1α/SIRT1 signaling pathway.
Animals ; PC12 Cells ; Rats ; Mitochondrial Dynamics/drug effects* ; Mitochondria/metabolism* ; Corticosterone/adverse effects* ; Membrane Potential, Mitochondrial/drug effects* ; Drugs, Chinese Herbal/pharmacology* ; Protective Agents/pharmacology* ; Cell Survival/drug effects*

Functional dyspepsia (FD), characterized by persistent or recurrent dyspeptic symptoms without identifiable organic, systemic or metabolic causes, is an increasingly recognized global health issue. The objective of this guideline is to equip clinicians and nursing professionals with evidence-based strategies for the management and treatment of adult patients with FD using traditional Chinese medicine (TCM). The Guideline Development Group consulted existing TCM consensus documents on FD and convened a panel of 35 clinicians to generate initial clinical queries. To address these queries, a systematic literature search was conducted across PubMed, EMBASE, the Cochrane Library, China National Knowledge Infrastructure (CNKI), VIP Database, China Biology Medicine (SinoMed) Database, Wanfang Database, Traditional Medicine Research Data Expanded (TMRDE), and the Traditional Chinese Medical Literature Analysis and Retrieval System (TCMLARS). The evidence from the literature was critically appraised using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. The strength of the recommendations was ascertained through a consensus-building process involving TCM and allopathic medicine experts, methodologists, pharmacologists, nursing specialists, and health economists, leveraging their collective expertise and empirical knowledge. The guideline comprises a total of 43 evidence-informed recommendations that span a range of clinical aspects, including the pathogenesis according to TCM, diagnostic approaches, therapeutic interventions, efficacy assessments, and prognostic considerations. Please cite this article as: Zhang SS, Zhao LQ, Hou XH, Bian ZX, Zheng JH, Tian HH, Yang GH, Hong WS, He YY, Liu L, Shen H, Li YP, Xie S, Shu J, Zeng BF, Li JX, Liu Z, Xiao ZH, Xiao JD, Zheng PY, Huang SG, Chen SL, Fei GJ. International clinical practice guideline on the use of traditional Chinese medicine for functional dyspepsia (2025). J Integr Med. 2025; 23(5):502-518.
Dyspepsia/drug therapy* ; Humans ; Medicine, Chinese Traditional/methods* ; Practice Guidelines as Topic ; Drugs, Chinese Herbal/therapeutic use*

Pregnancy complicated with acute myeloid leukemia is uncommon,requiring the collaborative management by specialists from departments of hematology,obstetrics,anesthesiology,and neonatology for both the parturient and the neonate.This article reports an anesthesic management process of a parturient woman with acute myeloid leukemia and reviews relevant literature published in recent years to systematically summarize the approach for anesthesia-related perinatal management of such patients.
Humans ; Female ; Pregnancy ; Leukemia, Myeloid, Acute/complications* ; Pregnancy Complications, Neoplastic ; Adult ; Anesthesia, Obstetrical/methods*

Objective To investigate the effect of cordyceps sinensis(CS)on the activation of fibroblasts through IL-6 trans-signaling pathway and its specific mechanism in the treatment of renal fibrosis.Methods Renal fibrosis mouse model was established by unilateral ischemia/reperfusion(UIR),and the mice were administered intragastrically CS,soluble glycoprotein 130 Fc(sgp130Fc)or Hyper-IL-6.Masson's trichrome staining was utilized to identify tubulointerstitial fibrosis.PAS staining was utilized to assess the extent of renal injury.Western blot was employed to analyze the expression levels of fibrosis markers[alpha-smooth muscle actin(α-SMA),fibronectin(FN)]and proteins associated with IL-6 trans-signaling pathway[phosphorylated signal transducer and activator of transcription 3(p-STAT3),soluble interleukin-6 receptor(sIL-6R)].The expression and localization of proteins were additionally detected by immunohistochemistry,immunofluorescence and qPCR.The effect of cordyceps sinensis extract cordycepin on IL-6 trans-signaling in fibroblasts was further investigated in vitro.Results The results from in vivo experiments showed that administration of CS during the chronic phase demonstrated a beneficial protective impact on inflammation and fibrosis in the affected kidney,and serum creatinine levels and collagen deposition were decreased.Western blot analysis revealed a decrease in the expression levels of α-SMA,FN,as well as IL-6 trans-signaling pathway protein p-STAT3,sIL-6R in the treatment group.Additionally,the mRNA expression levels of chemokines monocyte chemoattractant protein-1(MCP-1)and C-X-C motif chemokine ligand 12(CXCL12)were also decreased in the CS treatment group.Additionally,Hyper-IL-6 can partially counteract the therapeutic effects of CS.In vitro experiments further demonstrated that cordycepin inhibited the secretion of IL-6 from NRK-52E.Combined treatment of recombinant IL-6 and sIL-6R protein activated NRK-49F,leading to a significant increase in α-SMA,FN,and p-STAT3 expression levels.Cordycepin or sgp130Fc treatment significantly inhibited the proliferation of fibroblasts induced by IL-6 trans-signaling pathway.Conclusion CS can significantly reduce IL-6 secretion by renal tubular epithelial cells and inhibit the activation of IL-6 trans-signaling pathway in fibroblasts,thereby ameliorating renal interstitial fibrosis.