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 explore the mechanism of ligustil-ide(LIG)improving demyelination by inhibiting in-flammatory response in mice with distal middle cerebral artery occlusion(dMCAO)through AIM2/caspase-1 signal pathway.Methods Thirty C57BL/6N male mice were randomly divided into three groups:sham operation group(Sham group,n=10),model group(dMCAO group,n=10)and treatment group(LIG group,n=10).The dMCAO mouse model was estab-lished by electrocoagulation in dMCAO group and LIG group.The mice were scored by Longa after waking up,and the changes of cerebral blood flow were moni-tored by laser speckle blood flow imaging system after dMCAO.One hour after modeling,LIG(30 mg·kg-1·d-1)was injected intraperitoneally in LIG group,and the same amount of normal saline was injected in sham group and dMCAO group for one week until the end of the experiment.The mice in each group were stained with TTC,and the brain injury was observed pathologically.Fatigue turning bar test and open field test were used to evaluate the motor function and anxie-ty degree of mice,and then the brain tissues of mice were taken for black gold staining to compare the chan-ges of myelin sheath in each group.Immunofluores-cence staining was used to detect the average fluores-cence intensity of MBP,IBA1 and GFAP in CC,CPU and CX regions of mouse brains.ELISAwas used to de-tect the contents of TNF-α,IL-6,IL-1 β,IL-17A and BDNF in brain tissue proteins of mice.Western blot-ting was used to detect the protein expressions of AIM2,caspase-1 and ASC-in each group.Results Compared with the dMCAO group,the infarct area was reduced,the behavior was significantly improved and the demyelination was reduced in the LIG group.The expression of MBP protein in CC,CPU and CX regions increased(P＜0.05),the expression of IBA1 in CX decreased(P＜0.01),and the expression of GFAP in-creased in CC,CPU and CX regions(P＜0.01).The results of ELISA showed that the levels ofTNF-α(P＜0.01),IL-6(P＜0.01),IL-1β(P＜0.05)and IL-17A(P＜0.01)significantly decreased,while the ex-pression of BDNF increased(P＜0.05).The protein expression levels of AIM2,caspase-1 and ASC in mouse brain decreased after treatment(P＜0.01).Conclusion LIG has a protective effect on demyelina-tion in dMCAO mice,which may be related to the inhi-bition of AIM2/caspase-1 signaling pathway and in-flammation and to the promotion of BDNF secretion.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

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 explore the mechanism of ligustil-ide(LIG)improving demyelination by inhibiting in-flammatory response in mice with distal middle cerebral artery occlusion(dMCAO)through AIM2/caspase-1 signal pathway.Methods Thirty C57BL/6N male mice were randomly divided into three groups:sham operation group(Sham group,n=10),model group(dMCAO group,n=10)and treatment group(LIG group,n=10).The dMCAO mouse model was estab-lished by electrocoagulation in dMCAO group and LIG group.The mice were scored by Longa after waking up,and the changes of cerebral blood flow were moni-tored by laser speckle blood flow imaging system after dMCAO.One hour after modeling,LIG(30 mg·kg-1·d-1)was injected intraperitoneally in LIG group,and the same amount of normal saline was injected in sham group and dMCAO group for one week until the end of the experiment.The mice in each group were stained with TTC,and the brain injury was observed pathologically.Fatigue turning bar test and open field test were used to evaluate the motor function and anxie-ty degree of mice,and then the brain tissues of mice were taken for black gold staining to compare the chan-ges of myelin sheath in each group.Immunofluores-cence staining was used to detect the average fluores-cence intensity of MBP,IBA1 and GFAP in CC,CPU and CX regions of mouse brains.ELISAwas used to de-tect the contents of TNF-α,IL-6,IL-1 β,IL-17A and BDNF in brain tissue proteins of mice.Western blot-ting was used to detect the protein expressions of AIM2,caspase-1 and ASC-in each group.Results Compared with the dMCAO group,the infarct area was reduced,the behavior was significantly improved and the demyelination was reduced in the LIG group.The expression of MBP protein in CC,CPU and CX regions increased(P＜0.05),the expression of IBA1 in CX decreased(P＜0.01),and the expression of GFAP in-creased in CC,CPU and CX regions(P＜0.01).The results of ELISA showed that the levels ofTNF-α(P＜0.01),IL-6(P＜0.01),IL-1β(P＜0.05)and IL-17A(P＜0.01)significantly decreased,while the ex-pression of BDNF increased(P＜0.05).The protein expression levels of AIM2,caspase-1 and ASC in mouse brain decreased after treatment(P＜0.01).Conclusion LIG has a protective effect on demyelina-tion in dMCAO mice,which may be related to the inhi-bition of AIM2/caspase-1 signaling pathway and in-flammation and to the promotion of BDNF secretion.

Aim To investigate the anti-Zika virus(ZIKV)mechanism of diterpenoid compound 9 from Euphorbia helioscopia in vitro.Methods The cytotox-icity of compound 9 was evaluated using the CCK-8 as-say.A ZIKV-infected Vero cell model was established,and the antiviral activity was assessed through RT-qPCR,plaque assay,Western blot,and immunofluores-cence.Furthermore,the mechanism of action was elu-cidated using multi-cell line validation,nanoparticle tracking analysis,cellular thermal shift assay,and mo-lecular docking.Results In Vero cells,compound 9 exhibited an EC50 of(3.95±0.15)μmol·L-1 and a CC50 of(272.12±8.56)μmol·L-1,demonstrating significantly higher antiviral efficacy than the positive control drug ribavirin(RBV).Its virus inactivation effect was time-dependent and could significantly re-duce viral load and plaque formation.Studies revealed that compound 9 altered the physicochemical properties of ZIKV particles,including reducing surface charge and increasing particle size distribution.Additionally,it significantly enhanced the thermal stability of the prM protein.Molecular docking analysis indicated that compound 9 formed a high-affinity interaction with the prM protein(binding energy:-38.52 kJ·mol-1)and stabilized its structure through hydrophobic interac-tions.Conclusion Compound 9 exerts in vitro anti-ZIKV activity by directly inactivating the virus,disrup-ting viral particle integrity,and targeting the prM pro-tein.

Objective:To investigate the related factors of cognitive impairment in middle-aged and old-aged patients with type 2 diabetes mellitus(T2DM).Methods:A total of 970 patients with T2DM(585 middle-aged group and 385 old-aged group)were selected from residents of a large community in Beijing from September to December 2018.The Mini-Mental State Examination(MMSE)was used to assess the cognitive func-tion.Multivariate logistic regression was used to analyze the related factors.Results:The detection rates of cognitive impairment were 12.0％and 13.5％in middle-aged and old-aged patients with T2DM,respectively.Among mid-dle-aged patients with T2DM,work(OR=0.22,95％CI:0.03-0.77)and education at the junior college or un-dergraduate level and above(OR=0.18,95％CI:0.04-0.55)were protective factors for cognitive impair-ment.Myocardial infarction(OR=4.13,95％CI:1.26-13.63)was a risk factor for cognitive impairment.Among old-aged patients with T2DM,drinking tea 1-2 times a week(OR=0.11,95％CI:0.01-0.58)and education at the junior college or undergraduate level and above(OR=0.19,95％CI:0.05-0.54)were protective factors for cognitive impairment.Stroke(OR=3.64,95％CI:1.55-8.39)and good sleep self-assessment(OR=2.75,95％CI:1.13-7.35)were risk factors for cognitive impairment.Conclusion:Cognitive impairment in middle-aged pa-tients with T2DM is related to work,education level and myocardial infarction,and cognitive impairment in old-aged patients with T2DM is related to lifestyle,education level and stroke.

This study aims to explore the effects and action mechanisms of the active ingredients in Buyang Huanwu Decoction(BYHWD), namely tetramethylpyrazine(TMP) and hydroxy-safflor yellow A(HSYA), on oxygen-glucose deprivation/reglucose-reoxygenation(OGD/R)-induced inflammation and oxidative stress of microglia(MG). Network pharmacology was used to screen the effective monomer ingredients of BYHWD and determine the safe concentration range for each component. Inflammation and oxidative stress models were established to further screen the best ingredient combination and optimal concentration ratio with the most effective anti-inflammatory and antioxidant effects. OGD/R BV2 cell models were constructed, and BV2 cells in the logarithmic growth phase were divided into a normal group, a model group, an HSYA group, a TMP group, and an HSYA + TMP group. Enzyme-linked immunosorbent assay(ELISA) was used to detect the levels of inflammatory cytokines such as interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), and interleukin-6(IL-6). Oxidative stress markers, including superoxide dismutase(SOD), nitric oxide(NO), and malondialdehyde(MDA), were also measured. Western blot was used to analyze the protein expression of both inflammation-related pathway [Toll-like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)] and oxidative stress-related pathway [nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)]. Immunofluorescence was used to assess the expression of proteins such as inducible nitric oxide synthase(iNOS) and arginase-1(Arg-1). The most effective ingredients for anti-inflammatory and antioxidant effects in BYHWD were TMP and HSYA. Compared to the normal group, the model group showed significantly increased levels of IL-1β, TNF-α, IL-6, NO, and MDA, along with significantly higher protein expression of NF-κB, TLR4, Nrf2, and HO-1 and significantly lower SOD levels. The differences between the two groups were statistically significant. Compared to the model group, both the HSYA group and the TMP group showed significantly reduced levels of IL-1β, TNF-α, IL-6, NO, and MDA, lower expression of NF-κB and TLR4 proteins, higher levels of SOD, and significantly increased protein expression of Nrf2 and HO-1. Additionally, the expression of the M1-type MG marker iNOS was significantly reduced, while the expression of the M2-type MG marker Arg-1 was significantly increased. The results of the HSYA group and the TMP group had statistically significant differences from those of the model group. Compared to the HSYA group and the TMP group, the HSYA + TMP group showed further significant reductions in IL-1β, TNF-α, IL-6, NO, and MDA levels, along with significant reductions in NF-κB and TLR4 protein expression, an increase in SOD levels, and elevated Nrf2 and HO-1 protein expression. Additionally, the expression of the M1-type MG marker iNOS was reduced, while the M2-type MG marker Arg-1 expression increased significantly in the HSYA + TMP group compared to the TMP or HSYA group. The differences in the results were statistically significant between the HSYA + TMP group and the TMP or HSYA group. The findings indicated that the combined use of HSYA and TMP, the active ingredients of BYHWD, can effectively inhibit OGD/R-induced inflammation and oxidative stress of MG, showing superior effects compared to the individual use of either component.
Oxidative Stress/drug effects* ; Drugs, Chinese Herbal/pharmacology* ; Animals ; Mice ; Glucose/metabolism* ; Cell Line ; Inflammation/genetics* ; Oxygen/metabolism* ; Pyrazines/pharmacology* ; Microglia/metabolism* ; NF-E2-Related Factor 2/immunology* ; NF-kappa B/immunology* ; Toll-Like Receptor 4/immunology* ; Anti-Inflammatory Agents/pharmacology* ; Humans

Through a comprehensive analysis combining network pharmacology prediction and transcriptomics, this study systematically explained the multi-target mechanism of Cyanotis arachnoidea(CA) Gel in improving melasma. A melasma model was induced in female SD rats by progesterone injection combined with ultraviolet B(UVB) irradiation for 40 consecutive days, while the blank control group was only fed routinely. After successful model establishment, the rats were randomly divided into five groups and administered different doses of CA ethanol extract gel(high, medium, and low doses) or arbutin Gel(positive control), which were applied once daily for 28 consecutive days. Subsequently, the levels of superoxide dismutase(SOD), malondialdehyde(MDA), and tyrosinase(TYR) in the skin, serum, and liver tissues were measured. Hematoxylin-eosin(HE) staining and Masson-Fontana staining were used to observe the pathological changes in the tissues. Network pharmacology combined with transcriptomics was employed to identify core targets and pathways, and the differential gene expression was validated by quantitative real-time PCR(qPCR). Pharmacodynamic experiments showed that CA Gel significantly increased SOD activity and decreased MDA and TYR levels in the skin, serum, and liver of model rats. It also improved epidermal thickening, inflammatory infiltration, collagen loss, and melanin deposition. Network pharmacology analysis showed that CA mainly regulated core targets such as signal transducer and activator of transcription 3(STAT3), epidermal growth factor receptor(EGFR), and interleukin-6(IL-6), and modulated the phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT) and interleukin-17(IL-17) signaling pathways. Transcriptomic analysis showed that CA Gel significantly downregulated the gene expression of heat shock protein 90β family member 1(Hsp90b1), heat shock protein 90α family member 1(Hsp90aa1), and the key steroid synthesis enzyme cytochrome P450 family 17 subfamily A member 1(Cyp17a1), while upregulating thioredoxin 1(Txn1). qPCR results confirmed that CA Gel regulated oxidative stress and inflammatory response by inhibiting the IL-17 signaling pathway and steroid hormone synthesis. This study, for the first time, reveals the molecular mechanism of CA Gel in improving melasma through multi-target synergistic regulation of oxidative stress, inflammatory response, and hormone metabolism pathways, providing a scientific basis for the treatment of pigmentation diseases with traditional Chinese medicine.
Animals ; Rats ; Female ; Rats, Sprague-Dawley ; Network Pharmacology ; Drugs, Chinese Herbal/administration & dosage* ; Melanosis/metabolism* ; Transcriptome/drug effects* ; Humans ; Superoxide Dismutase/genetics* ; Signal Transduction/drug effects* ; Malondialdehyde/metabolism*

This study compared the differences in intestinal absorption characteristics of eleven active components in Rubus multibracteatus(RM) extract(protocatechuic acid, tiliroside, scutellarin, luteoloside, astragalin, epicatechin, catechin, xanthotoxin, p-coumaric acid, caffeic acid, and apigenin-7-O-glucuronide) between normal rats and inflammatory pain model rats using the in-vitro everted intestinal sac model. The RM extract was administered at absorption concentrations of 25.0, 50.0, and 100.0 mg·mL~(-1). The contents of the eleven components in intestinal absorption solution samples were quantified by ultra-performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS), and their cumulative absorption(Q) and absorption rate constant(K_a) were calculated to evaluate the absorption characteristics of these components in normal rats and inflammatory pain model rats. The results show that except for catechin, epicatechin, and caffeic acid, the cumulative absorption-time curves of the other eight components(protocatechuic acid, tiliroside, scutellarin, luteoloside, astragalin, xanthotoxin, p-coumaric acid, and apigenin-7-O-glucuronide) exhibit an upward trend without saturation, with correlation coefficients(R~2) all > 0.9, indicating linear absorption. However, the overall absorption of all components is not dose-dependent with increasing concentration, suggesting that their absorption mechanisms are not solely passive diffusion. In both normal and model rats, the jejunum shows the highest absorption for all components except xanthotoxin. The overall absorption of seven components(excluding protocatechuic acid, caffeic acid, apigenin-7-O-glucuronide, and luteoloside) in normal rats is better than that in model rats across all intestinal segments. These findings indicate that the pathological state of inflammatory pain alters the intestinal absorption of RM extract, and its mechanism needs further investigation.
Animals ; Rats ; Intestinal Absorption/drug effects* ; Male ; Rats, Sprague-Dawley ; Drugs, Chinese Herbal/metabolism* ; Disease Models, Animal ; Pain/metabolism* ; Intestines/drug effects* ; Intestinal Mucosa/metabolism*