Objective:To investigate the distribution of iodine in drinking water in external environment and the iodine nutrition status of key population in Guizhou Province, and to provide a basis for further precise implementation of prevention and control strategy of "adapting to local conditions, providing classified guidance, and scientifically supplementing iodine".Methods:From April to September 2023, a survey on the iodine level of residents' drinking water was conducted in administrative villages (neighborhood committees, hereafter referred to as administrative village) in 88 counties (districts) of 9 cities (prefectures) in Guizhou Province. At the same time, one township (town) was selected from each of the five districts of east, west, south, north and center of each county (district). From each township (town), 40 non-boarding students aged 8 - 10 years old from one primary school and 20 pregnant women were selected. Household edible salt sample and once random urine sample were collected for detection of salt iodine and urinary iodine levels.Results:The survey covered 16 492 administrative villages in 1 481 townships (towns), 88 counties (districts), 9 cities (prefectures) throughout the province. A total of 51 531 samples of residents' drinking water were collected, with a median water iodine level of 1.50 μg/L and a range of 0.01 - 98.70 μg/L. Among them, there were 16 284, 208, and 0 administrative villages with median water iodine levels < 10, 10 - < 40, and 40 - 100 μg/L, respectively, accounting for 98.74%, 1.26%, and 0, respectively. A total of 26 491 samples of household edible salt were collected from children and pregnant women, with a median salt iodine levels of 27.6 mg/kg. The coverage rate of iodized salt was 99.6% (26 395/26 491), and the qualified iodized salt consumption rate was 97.0% (25 708/26 491). And 17 657 urine samples from children and 8 834 urine samples from pregnant women were collected, with median urinary iodine levels of 222.1 and 164.4 μg/L, respectively. There were statistically significant differences in urinary iodine levels among children of different genders and ages ( Z = - 6.08, H = 19.17, P < 0.001). The results of correlation analysis showed that there was no correlation between urinary iodine of children and pregnant women and water iodine ( r = 0.01 0.02, P > 0.05), while urinary iodine of pregnant women was positively correlated with salt iodine ( r = 0.02, P = 0.041). Conclusions:The external environment of Guizhou Province is generally deficient in iodine. Under the universal salt iodization policy, children have sufficient iodine nutrition, and pregnant women have an appropriate level of iodine nutrition. Comprehensive prevention and control measures, mainly based on universal salt iodization, should be continuously carried out to eliminate the harm of iodine deficiency.

Experimental teaching is an important component of the course Medical Immunology,which requires the use of experimental animals and the execution of experimental animals by medical students.By applying the carbon dioxide euthanasia system,it can effectively reduce the pain of experimental animals,ensure their welfare,and meet ethical requirements.It can also improve the efficiency of experimental teaching in Medical Immunology,reduce environmental pollution,and promote medical students to estab-lish scientific values and worldviews that pay attention to experimental animals and respect life,which is conducive to becoming future medical service talents.In the experimental teaching of Medical Immunology,the appropriate application of carbon dioxide euthanasia system combined with effective ideological and political construction of the curriculum can further implement the Party's educational policy of cultivating morality and talents,and lay a good foundation for cultivating medical talents with comprehensive knowledge,high skills and excellent quality.

OBJECTIVE To investigate the analgesic effects and potential mechanisms of the partial agonist of the 5-hydroxytryptamine 1A(5-HT1A)receptor and the selective 5-HT reuptake inhibitor,viladazone(Vil),in various animal models of pain.METHODS ① Mouse acetic acid writhing test:KM mice were divided into the model group,model+morphine 10 mg·kg-1 group,and model+Vil 2,4,8 mg·kg-1 groups.Thirty minutes after ig administration of saline(model group)or corresponding drugs,each group was ip injected with a 2%acetic acid aqueous solution(0.01 mL·g-1),and the writhing frequency of the mice was observed and recorded from 5 to 20 min.② Mouse formalin pain test:KM mice were divided into the model group and model+Vil 2,4 and 8 mg·kg-1 groups.Thirty minutes after ig adminis-tration of saline(model group)or drugs,20 μL of 5%formalin solution was sc injected into the right plantar region of the mice.The licking time(the sum of the duration of licking and biting the paw)of the mice was observed and recorded during two periods:the acute phase(0-5 min after sc formalin injec-tion)and the delayed phase(15-35 min after sc formalin injection).③ Rat chronic constriction injury(CCI)of the sciatic nerve experiment:SD rats successfully examined with a paw withdrawal threshold(PWT)<5 g were randomly divided into a CCI model group and a CCI model+Vil 2,4 and 8 mg·kg-1 group.Solvent(model group)or corresponding drugs were ig administered,and the PWT of the modeled side was measured at 30,60,120 and 240 min after the first administration to evaluate the acute anal-gesic effect of Vil on mechanical pain.Then,Vil was continuously ig administered for 14 d,and the PWT was measured 1 h after Vil administration on the 7th and 14th d to evaluate the long-term analgesic effect of Vil.Immunofluorescence staining was employed to analyze the expression levels of inflamma-tion-related proteins,ionized calcium binding adapter molecule 1(IBA-1),tumor necrosis factor α(TNF-α),and interleukin 1β(IL-1β),in brain tissues.Enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of IBA-1,TNF-α and IL-1β in the dorsal root ganglion of the spinal cord in the CCI model.RESULTS ① In the mouse model of acetic acid writhing,single ig administration of morphine 10 mg·kg-1 and Vil at varied doses significantly reduced the number of writhings induced by acetic acid compared to the model group.② In the formalin-induced pain model,the average licking time of the model group was 50.5 s during the acute phase of inflammatory pain(0-5 min after intraplantar injec-tion of 5%formalin),and 347.9 s during the delayed phase of inflammatory pain(25-35 min after formalin injection).Compared to the model group,single ig administration of Vil 2-8 mg·kg-1 reduced chronic pain induced by formalin in mice,and each dose of Vil significantly decreased the licking time of mice,but had no notable impact on the licking duration exhibited by mice during acute phase.③ In the CCI model,the PWT values of CCI model rats significantly decreased compared with the control group.Pathological damage to varying extents was observed in brain slices,manifested as enlarged intercellular spaces and the appearance of vacuoles.The expression of IBA-1 in brain tissue significantly increased,while TNF-α and IL-1β hardly changed.The levels of IBA-1,TNF-α and IL-1β in the spinal dorsal root ganglion significantly increased.Compared with the CCI model,after single administration of Vil 2-8 mg·kg-1 for 60,120 and 240 min,Vil significantly reduced the PWT values.After two-week continuous administration,the PWT values in Vil 4 and 8 mg·kg-1 were significantly reduced,and Vil 2-8 mg·kg-1 could alleviate the neuropathic pain to some extent.Vil 8 mg·kg-1 significantly reduced the elevated levels of inflammatory factors compared to CCI rats.CONCLUSION The antidepressant Vil exhibits analgesic effects in mouse models of acetic acid writhing,formalin-induced inflammation,and neuropathic pain induced by CCI in rats,with a more pronounced effect on neuropathic pain.The mechanism of action may be related to the inhibition of inflammatory pathways of IBA-1.

Objective:To evaluate the role of the CC chemokine ligand 2/CC chemokine receptor 2 (CCL2/CCR2) signaling pathway in electroacupuncture (EA)-induced reduction of spinal cord injury (SCI) in rats.Methods:Sixty clean-grade healthy adult female Sprague-Dawley rats, weighing 210-250 g, were divided into 5 groups ( n=12 each) using a random number table method: sham operation group (group S), group SCI, SCI+ Anti-CCL2 group (group SCI+ A), SCI+ EA group (group SCI+ EA), and spinal cord injury+ EA+ rCCL2 group (group SCI+ EA+ R). The SCI model was established using the Allen method in anesthetized animals. Group S only underwent spinous process and laminectomy without damaging the spinal cord. In SCI+ A group, CCL2 neutralizing antibody 50 μg/kg was intrathecally injected at 0, 3 and 6 days after successful development of the SCI model. On the 7th day after the successful development of the SCI model, Jiaji, Dazhui and Mingmen acupoints were stimulated with a depth of 2 mm, voltage of 12-15 mV and frequency of 2 Hz for 30 min once a day for 7 consecutive days in SCI+ EA group. In SCI+ EA+ R group, recombinant rat CCL2 2.5 μg/kg was intrathecally injected at the site of injury at 0, 3 and 6 days after successful development of the SCI model, and the remaining treatments were similar to those in SCI+ EA group. At 1 day before developing the model, 0, 3, 7, 14, 21 and 28 days after developing the model, the mechanical paw withdraw threshold (MWT) and thermal paw withdrawal latency (TWL) were measured, and the motor function was assessed by BBB score. The rats were sacrificed after the final behavioral testing, and their spinal cord tissues were obtained for determination of the expression of CCL2 and CCR2 protein and mRNA (by Western blot or quantitative real-time polymerase chain reaction), the expression of GFAP (by immunofluorescence), contents of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 (by enzyme-linked immunosorbent assay) and for examination of the pathological changes (using HE staining). Results:Compared with S group, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model, the expression of CCL2 and CCR2 protein and mRNA and GFAP was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI group ( P<0.05). Compared with SCI group, the MWT and BBB scores were significantly increased, and the TWL was prolonged at 7 days after developing the model in SCI+ A group, the MWT and BBB scores were significantly increased, and the TWL was prolonged at 14 days after developing the model in SCI+ EA group, and the expression of CCL2 and CCR2 protein and mRNA and GFAP was significantly down-regulated, and the contents of TNF-α, IL-1β and IL-6 were decreased in SCI+ A and SCI+ EA groups ( P<0.05). Compared with SCI+ EA group, the MWT and BBB scores were significantly decreased at 14 days after developing the model, the TWL was shortened, the expression of CCL2 and CCR2 protein and mRNA and GFAP was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI+ EA+ R group ( P<0.05). Compared with SCI+ A and SCI+ EA groups, the histopathological injury were significantly attenuated in SCI group, and the histopathological injury was aggravated in SCI+ EA+ R group. Conclusions:The CCL2/CCR2 signaling pathway is involved in the process by which EA reduces SCI, and the mechanism is related to the inhibition of astrocyte activation, thereby reducing the inflammatory response.

Objective:To evaluate the effect of electroacupuncture (EA) on ionotropic purinergic receptor 4 (P2X4R)/nuclear factor-kappa B (NF-κB) signaling pathway during spinal cord injury (SCI) in rats.Methods:Thirty-six clean-grade healthy adult female Sprague-Dawley rats, weighing 210-250 g, were divided into 3 groups ( n=12 each) using a random number table method: sham surgery group (S group), SCI group, and SCI+ EA treatment group (SCI+ EA group). The SCI model was established by the Allen′s method in anesthetized animals. In group S, only the spinous processes and vertebral laminae were resected, but the spinal cord was not injured. On the 7th day after developing the model, EA of Jiaji, Dazhui, and Mingmen lasting 30 min was performed once a day for 7 consecutive days, with a depth of 2 mm, intensity of 12-15 mV, frequency of 2 Hz, in SCI+ EA group. The mechanical paw withdraw threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before developing the model and 3, 7, 14, 21 and 28 days after developing the model, and the motor function was assessed using the Basso-Beattie-Bresnahan (BBB) score. The recovery of motor function was assessed using footprint analysis at 28 days after developing the model. After the final behavioral testing, the rats were sacrificed, and spinal cord tissues were harvested to observe the pathological changes of the spinal cord tissues using hematoxylin-eosin staining, to detect the expression of P2X4R and phosphorylated NF-κB p65 (p-NF-κB p65) (by immunohistochemical analysis and Western blot) and to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 (by enzyme-linked immunosorbent assay). Results:Compared with the baseline measured at 1 day before developing the model, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model in SCI group and SCI+ EA group ( P<0.05). Compared with S group, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model, the expression of P2X4R and p-NF-κB p65 in spinal cord tissues was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI group ( P<0.05). Compared with SCI group, the MWT and BBB scores were significantly increased and the TWL was prolonged at 14, 21 and 28 days after developing the model, the expression of P2X4R and p-NF-κB p65 in spinal cord tissues was down-regulated, and the contents of TNF-α, IL-1β and IL-6 were decreased ( P<0.05), and the pathological damage of spinal cord tissues was alleviated and footprints were reduced in SCI+ EA group. Conclusions:The mechanism by which EA alleviates SCI may be related to the inhibition of the activation of the P2X4R/NF-κB signaling pathway and the reduction in the inflammatory response in rats.

A throat swab sample from a pediatric case in Tongzhou District, Beijing was identified as enterovirus; the patient was a 1-year-and-8-month-old male sporadic case. Whole-genome sequencing revealed a viral genome length of 7 436 bp. BLAST alignment confirmed the serotype as EV-D68. Phylogenetic analysis of the whole genome indicated that this strain belongs to the B3 clade, showing closer genetic proximity to the 2018 Shanghai strain MW697453 with 99.53% whole-genome nucleotide homology. Genetic and amino acid variation analysis demonstrated that the B3 subclade to which this strain belongs exhibits a nucleotide deletion at positions 718–726, differing from deletion sites observed in other B3 clade strains. A key neuropathogenic amino acid site, T650A, was found to have undergone mutation. Recombination analysis confirmed no cross-clade recombination events in this strain. This study conducted genetic characterization of the strain's evolutionary relationship with EV-D68 strains from different regions and years in China, providing data support for formulating prevention and control measures against EV-D68 infection.

Objective:To evaluate the role of the CC chemokine ligand 2/CC chemokine receptor 2 (CCL2/CCR2) signaling pathway in electroacupuncture (EA)-induced reduction of spinal cord injury (SCI) in rats.Methods:Sixty clean-grade healthy adult female Sprague-Dawley rats, weighing 210-250 g, were divided into 5 groups ( n=12 each) using a random number table method: sham operation group (group S), group SCI, SCI+ Anti-CCL2 group (group SCI+ A), SCI+ EA group (group SCI+ EA), and spinal cord injury+ EA+ rCCL2 group (group SCI+ EA+ R). The SCI model was established using the Allen method in anesthetized animals. Group S only underwent spinous process and laminectomy without damaging the spinal cord. In SCI+ A group, CCL2 neutralizing antibody 50 μg/kg was intrathecally injected at 0, 3 and 6 days after successful development of the SCI model. On the 7th day after the successful development of the SCI model, Jiaji, Dazhui and Mingmen acupoints were stimulated with a depth of 2 mm, voltage of 12-15 mV and frequency of 2 Hz for 30 min once a day for 7 consecutive days in SCI+ EA group. In SCI+ EA+ R group, recombinant rat CCL2 2.5 μg/kg was intrathecally injected at the site of injury at 0, 3 and 6 days after successful development of the SCI model, and the remaining treatments were similar to those in SCI+ EA group. At 1 day before developing the model, 0, 3, 7, 14, 21 and 28 days after developing the model, the mechanical paw withdraw threshold (MWT) and thermal paw withdrawal latency (TWL) were measured, and the motor function was assessed by BBB score. The rats were sacrificed after the final behavioral testing, and their spinal cord tissues were obtained for determination of the expression of CCL2 and CCR2 protein and mRNA (by Western blot or quantitative real-time polymerase chain reaction), the expression of GFAP (by immunofluorescence), contents of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 (by enzyme-linked immunosorbent assay) and for examination of the pathological changes (using HE staining). Results:Compared with S group, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model, the expression of CCL2 and CCR2 protein and mRNA and GFAP was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI group ( P<0.05). Compared with SCI group, the MWT and BBB scores were significantly increased, and the TWL was prolonged at 7 days after developing the model in SCI+ A group, the MWT and BBB scores were significantly increased, and the TWL was prolonged at 14 days after developing the model in SCI+ EA group, and the expression of CCL2 and CCR2 protein and mRNA and GFAP was significantly down-regulated, and the contents of TNF-α, IL-1β and IL-6 were decreased in SCI+ A and SCI+ EA groups ( P<0.05). Compared with SCI+ EA group, the MWT and BBB scores were significantly decreased at 14 days after developing the model, the TWL was shortened, the expression of CCL2 and CCR2 protein and mRNA and GFAP was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI+ EA+ R group ( P<0.05). Compared with SCI+ A and SCI+ EA groups, the histopathological injury were significantly attenuated in SCI group, and the histopathological injury was aggravated in SCI+ EA+ R group. Conclusions:The CCL2/CCR2 signaling pathway is involved in the process by which EA reduces SCI, and the mechanism is related to the inhibition of astrocyte activation, thereby reducing the inflammatory response.

Objective:To evaluate the effect of electroacupuncture (EA) on ionotropic purinergic receptor 4 (P2X4R)/nuclear factor-kappa B (NF-κB) signaling pathway during spinal cord injury (SCI) in rats.Methods:Thirty-six clean-grade healthy adult female Sprague-Dawley rats, weighing 210-250 g, were divided into 3 groups ( n=12 each) using a random number table method: sham surgery group (S group), SCI group, and SCI+ EA treatment group (SCI+ EA group). The SCI model was established by the Allen′s method in anesthetized animals. In group S, only the spinous processes and vertebral laminae were resected, but the spinal cord was not injured. On the 7th day after developing the model, EA of Jiaji, Dazhui, and Mingmen lasting 30 min was performed once a day for 7 consecutive days, with a depth of 2 mm, intensity of 12-15 mV, frequency of 2 Hz, in SCI+ EA group. The mechanical paw withdraw threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before developing the model and 3, 7, 14, 21 and 28 days after developing the model, and the motor function was assessed using the Basso-Beattie-Bresnahan (BBB) score. The recovery of motor function was assessed using footprint analysis at 28 days after developing the model. After the final behavioral testing, the rats were sacrificed, and spinal cord tissues were harvested to observe the pathological changes of the spinal cord tissues using hematoxylin-eosin staining, to detect the expression of P2X4R and phosphorylated NF-κB p65 (p-NF-κB p65) (by immunohistochemical analysis and Western blot) and to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 (by enzyme-linked immunosorbent assay). Results:Compared with the baseline measured at 1 day before developing the model, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model in SCI group and SCI+ EA group ( P<0.05). Compared with S group, the MWT and BBB scores were significantly decreased and the TWL was shortened at each time point after developing the model, the expression of P2X4R and p-NF-κB p65 in spinal cord tissues was up-regulated, and the contents of TNF-α, IL-1β and IL-6 were increased in SCI group ( P<0.05). Compared with SCI group, the MWT and BBB scores were significantly increased and the TWL was prolonged at 14, 21 and 28 days after developing the model, the expression of P2X4R and p-NF-κB p65 in spinal cord tissues was down-regulated, and the contents of TNF-α, IL-1β and IL-6 were decreased ( P<0.05), and the pathological damage of spinal cord tissues was alleviated and footprints were reduced in SCI+ EA group. Conclusions:The mechanism by which EA alleviates SCI may be related to the inhibition of the activation of the P2X4R/NF-κB signaling pathway and the reduction in the inflammatory response in rats.

A throat swab sample from a pediatric case in Tongzhou District, Beijing was identified as enterovirus; the patient was a 1-year-and-8-month-old male sporadic case. Whole-genome sequencing revealed a viral genome length of 7 436 bp. BLAST alignment confirmed the serotype as EV-D68. Phylogenetic analysis of the whole genome indicated that this strain belongs to the B3 clade, showing closer genetic proximity to the 2018 Shanghai strain MW697453 with 99.53% whole-genome nucleotide homology. Genetic and amino acid variation analysis demonstrated that the B3 subclade to which this strain belongs exhibits a nucleotide deletion at positions 718–726, differing from deletion sites observed in other B3 clade strains. A key neuropathogenic amino acid site, T650A, was found to have undergone mutation. Recombination analysis confirmed no cross-clade recombination events in this strain. This study conducted genetic characterization of the strain's evolutionary relationship with EV-D68 strains from different regions and years in China, providing data support for formulating prevention and control measures against EV-D68 infection.

OBJECTIVE To investigate the analgesic effects and potential mechanisms of the partial agonist of the 5-hydroxytryptamine 1A(5-HT1A)receptor and the selective 5-HT reuptake inhibitor,viladazone(Vil),in various animal models of pain.METHODS ① Mouse acetic acid writhing test:KM mice were divided into the model group,model+morphine 10 mg·kg-1 group,and model+Vil 2,4,8 mg·kg-1 groups.Thirty minutes after ig administration of saline(model group)or corresponding drugs,each group was ip injected with a 2%acetic acid aqueous solution(0.01 mL·g-1),and the writhing frequency of the mice was observed and recorded from 5 to 20 min.② Mouse formalin pain test:KM mice were divided into the model group and model+Vil 2,4 and 8 mg·kg-1 groups.Thirty minutes after ig adminis-tration of saline(model group)or drugs,20 μL of 5%formalin solution was sc injected into the right plantar region of the mice.The licking time(the sum of the duration of licking and biting the paw)of the mice was observed and recorded during two periods:the acute phase(0-5 min after sc formalin injec-tion)and the delayed phase(15-35 min after sc formalin injection).③ Rat chronic constriction injury(CCI)of the sciatic nerve experiment:SD rats successfully examined with a paw withdrawal threshold(PWT)<5 g were randomly divided into a CCI model group and a CCI model+Vil 2,4 and 8 mg·kg-1 group.Solvent(model group)or corresponding drugs were ig administered,and the PWT of the modeled side was measured at 30,60,120 and 240 min after the first administration to evaluate the acute anal-gesic effect of Vil on mechanical pain.Then,Vil was continuously ig administered for 14 d,and the PWT was measured 1 h after Vil administration on the 7th and 14th d to evaluate the long-term analgesic effect of Vil.Immunofluorescence staining was employed to analyze the expression levels of inflamma-tion-related proteins,ionized calcium binding adapter molecule 1(IBA-1),tumor necrosis factor α(TNF-α),and interleukin 1β(IL-1β),in brain tissues.Enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of IBA-1,TNF-α and IL-1β in the dorsal root ganglion of the spinal cord in the CCI model.RESULTS ① In the mouse model of acetic acid writhing,single ig administration of morphine 10 mg·kg-1 and Vil at varied doses significantly reduced the number of writhings induced by acetic acid compared to the model group.② In the formalin-induced pain model,the average licking time of the model group was 50.5 s during the acute phase of inflammatory pain(0-5 min after intraplantar injec-tion of 5%formalin),and 347.9 s during the delayed phase of inflammatory pain(25-35 min after formalin injection).Compared to the model group,single ig administration of Vil 2-8 mg·kg-1 reduced chronic pain induced by formalin in mice,and each dose of Vil significantly decreased the licking time of mice,but had no notable impact on the licking duration exhibited by mice during acute phase.③ In the CCI model,the PWT values of CCI model rats significantly decreased compared with the control group.Pathological damage to varying extents was observed in brain slices,manifested as enlarged intercellular spaces and the appearance of vacuoles.The expression of IBA-1 in brain tissue significantly increased,while TNF-α and IL-1β hardly changed.The levels of IBA-1,TNF-α and IL-1β in the spinal dorsal root ganglion significantly increased.Compared with the CCI model,after single administration of Vil 2-8 mg·kg-1 for 60,120 and 240 min,Vil significantly reduced the PWT values.After two-week continuous administration,the PWT values in Vil 4 and 8 mg·kg-1 were significantly reduced,and Vil 2-8 mg·kg-1 could alleviate the neuropathic pain to some extent.Vil 8 mg·kg-1 significantly reduced the elevated levels of inflammatory factors compared to CCI rats.CONCLUSION The antidepressant Vil exhibits analgesic effects in mouse models of acetic acid writhing,formalin-induced inflammation,and neuropathic pain induced by CCI in rats,with a more pronounced effect on neuropathic pain.The mechanism of action may be related to the inhibition of inflammatory pathways of IBA-1.