OBJECTIVE To establish an in vitro inflammatory model of BV2 by observing the activity,the release amount of NO and the expression of inflammatory factors of microglial cells(BV2)induced by lipopolysaccharides(LPS).ME...OBJECTIVE To establish an in vitro inflammatory model of BV2 by observing the activity,the release amount of NO and the expression of inflammatory factors of microglial cells(BV2)induced by lipopolysaccharides(LPS).METHODS BV2 was routinely cultured in vitro.Cell viability was measured by CCK-8 meth⁃od.And by drew cell growth curve to determine the logarithmic growth cycle of the cells.After 24 h of routine culture,BV2 were induced by adding different concentrations of LPS(0.1,1.0 and 10.0 mg·L-1)for 4,8,12,24 and 48 h,respectively.Meanwhile,the morphological changes of BV2 were observed under inverted microscope to compare the activation degree of microglia at dif⁃ferent time and concentration.Cell activity and nitric oxide(NO)level were determined by CCK-8 and Griess method respectively,which could help to determine the optimal concentration and time of modeling.Finally,It were determined by ELISA that the concentrations of tumor necrosis factorα(TNF-α),interleukin-6(IL-6)and IL-1βin supernatant of LPS 1 mg·L-1 culture for 24 h.RESULTS BV2 were in logarithmic growth phase for 1 to 3 d after subculture.LPS 1 mg·L-1 induced BV2 for 24 or 48 h which could increase the release amount of NO significantly(P<0.05).In order to save time,LPS induced BV2 for 24 h were selected for subsequent experiments.Microglial cells in resting state were observed to be elongated spindle shape under inverted micro⁃scope.After LPS activation,the cell body became larger and the branching processes shrank back,presenting an amoeba-like appearance.ELISA results showed that the concentrations of TNF-α,IL-6 and IL-1βin supernatant of LPS 1 mg·L-1 cultured for 24 h were significantly increased which compared with the control group(P<0.05).CONCLUSION LPS could induce the activation of BV2 and up-regulate the level of inflammatory factors.The optimal condition for establishing stable BV2 microglial inflammatory model was used LPS 1 g·L-1 induced for 24 h.展开更多
Using inducers to induce cells to produce inflammatory response is a common in vitro experimental method to study inflammation.However,there are relatively few inflammatory models developed for the cosmetic industry,a...Using inducers to induce cells to produce inflammatory response is a common in vitro experimental method to study inflammation.However,there are relatively few inflammatory models developed for the cosmetic industry,and there are also great differences in the control of model induction,the selection of inflammatory indicators,and the concentration of inducers.Therefore,in this paper,by systematically studying the effects of Lipopolysaccharide(LPS)on the cell viability,the levels of IL-1α,IL-8 and ROS of human primary keratinocytes,a skin inflammation model based human primary keratinocyte was developed.The results showed that 0.01~100μg/mL LPS had no significant effect on the cell viability of human primary keratinocytes,while 100μg/mL LPS could simultaneously induce human primary keratinocytes to produce large amounts of IL-1αand IL-8,and 0.01μg/mL LPS could induce plentiful ROS.Therefore,a skin inflammation model for differential induction of different inflammatory indicators was established,and the sample OSM2021041301 was tested with this model,it was found that sample OSM2021041301 could significantly inhibit LPS-induced elevated IL-1αand IL-8 levels,the inhibitory effect on LPS-induced elevated ROS level was weak.The results indicated that OSM2021041301 has certain anti-inflammatory effect on inflammation caused by the increase of IL-1α,IL-8 and ROS induced by LPS and its analogues.展开更多
Periodontitis is an inflammatory autoimmune disease. Treatment should alleviate inflammation, regulate the immune reaction and promote periodontal tissue regeneration. Icariin is the main active ingredient of Epimedii...Periodontitis is an inflammatory autoimmune disease. Treatment should alleviate inflammation, regulate the immune reaction and promote periodontal tissue regeneration. Icariin is the main active ingredient of Epimedii Folium, and it is a promising compound for the enhancement of mesenchymal stem cell function, promotion of bone formation, inhibition of bone resorption, alleviation of inflammation and regulation of immunity. The study investigated the effect of icariin on periodontal tissue regeneration in a minipig model of periodontitis. The minipig model of periodontitis was established. Icariin was injected locally. The periodontal clinical assessment index, a computed tomography(CT) scan, histopathology and enzyme-linked immune sorbent assay(ELISA)were used to evaluate the effects of icariin. Quantitative analysis results 12 weeks post-injection demonstrated that probing depth,gingival recession, attachment loss and alveolar bone regeneration values were(3.72 ± 1.18) mm vs.(6.56 ± 1.47) mm,(1.67 ± 0.59)mm vs.(2.38 ± 0.61) mm,(5.56 ± 1.29) mm vs.(8.61 ± 1.72) mm, and(25.65 ± 5.13) mm3 vs.(9.48 ± 1.78) mm3 in the icariin group and0.9% NaCl group, respectively. The clinical assessment, CT scan, and histopathology results demonstrated significant enhancement of periodontal tissue regeneration in the icariin group compared to the 0.9% NaCl group. The ELISA results suggested that the concentration of interleukin-1 beta(IL-1β) in the icariin group was downregulated compared to the 0.9% NaCl group, which indicates that local injection of icariin relieved local inflammation in a minipig model of periodontitis. Local injection of icariin promoted periodontal tissue regeneration and exerted anti-inflammatory and immunomodulatory function. These results support the application of icariin for the clinical treatment of periodontitis.展开更多
Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea（OSA）.We used a well-described OSA rat model induced with simultan...Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea（OSA）.We used a well-described OSA rat model induced with simultaneous intermittent hypoxia.Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled.The rats were exposed to intermittent hypoxia 8 hours daily for 5weeks.The changes of cardiac structure and function were examined by ultrasound.The cardiac pathology,apoptosis,and fibrosis were analyzed by H＆E staining,TUNNEL assay,and picosirius staining,respectively.The expression of inflammation and fibrosis marker genes was analyzed by quantitative real-time PCR and Western blot.Chronic intermittent hypoxia/low pressure resulted in significant increase of left ventricular internal diameters（LVIDs）,endsystolic volume（ESV）,end-diastolic volume（EDV）,and blood lactate level and marked reduction in ejection fraction and fractional shortening.Chronic intermittent hypoxia increased TUNNEL-positive myocytes,disrupted normal arrangement of cardiac fibers,and increased Sirius stained collagen fibers.The expression levels of hypoxia induced factor（HIF）-l α,NF-κB,IL-6,and matrix metallopeptidase 2（MMP-2） were significantly increased in the heart of rats exposed to chronic intermittent hypoxia.In conclusion,the left ventricular function was adversely affected by chronic intermittent hypoxia,which is associated with increased expression of HIF-lα and NF-κB signaling molecules and development of cardiac inflammation,apoptosis and fibrosis.展开更多
In order to investigate the effects of interleukin-18 （IL-18） on airway inflammation and the Th1/Th2 cytokine balance in guinea pig asthmatic model as well as its possible mechanisms, the asthmatic model was establi...In order to investigate the effects of interleukin-18 （IL-18） on airway inflammation and the Th1/Th2 cytokine balance in guinea pig asthmatic model as well as its possible mechanisms, the asthmatic model was established by intraperitoneal injection of ovalbumin （OVA） and aerosol challenges into guinea pigs, and 30 treated animals were randomly divided into three groups of 10 animals in each groups, in which group A served as the asthmatic model, group B as the controls and group C as the group treated with IL-18. The counting and categorization of the inflammatory cells in bronchoalveolar lavage fluid （BALF） were performed by using light microscopy, and the contents of cytokines （ IFN-γ, IL- 2, IL-4 and IL-5） were assayed by means of the ELISA kit. The experimental results showed that the numbers of eosinophils （ESO） in BALF of group A, B and C were （97.70 ± 58.03） × 10^6/L, （11.68 × 9.95） × 10^6/L and （28.62 ± 10.46） × 10^6/L, respectively, in which the number of eosinophils in group A was significantly higher than those of group B and C. Also, the number of neutrophils in BALF of group A was even higher than those in group B and C. In addition, the contents of IFN-7 and IL-2 in group A were lower than those in group B and C, but the contents of IL-4 as well as IL-5 were rather higher than those in group B and C. It is evident from the above observations that IL-18 can effectively inhibit the asthmatic inflammatory cells in BALF with an imbalance of the Thl/Th2 cytokines, thus offer- ing the experimental basis for the clinical application of IL-18 in the prevention and treatment of asthma.展开更多
CD93 and GAIP-interacting protein, C termius （GIPC） have been shown to interactively alter phagocytic processes of immune cells. CD93 and GIPC expression and localization during cen-tral nervous system inflammation ...CD93 and GAIP-interacting protein, C termius （GIPC） have been shown to interactively alter phagocytic processes of immune cells. CD93 and GIPC expression and localization during cen-tral nervous system inflammation have not yet been reported. In this study, we established a rat model of brain inlfammation by lipopolysaccharide injection to the lateral ventricle. In the brain of rats with inlfammation, western blots showed increased CD93 expression that decreased over time. GIPC expression was unaltered. Immunohistochemistry demonstrated extensive distribution of CD93 expression mainly in cell membranes in the cerebral cortex. After lipopoly-saccharide stimulation, CD93 expression increased and then reduced, with distinct staining in the cytoplasm and nucleus. Double immunolfuorescence staining in cerebral cortex of normal rats showed that CD93 and GIPC widely expressed in resting microglia and neurons. CD93 was mainly expressed in microglial and neuronal cell membranes, while GIPC was expressed in both cell membrane and cytoplasm. In the cerebral cortex at 9 hours after model establishment, CD93-immunoreactive signal diminished in microglial membrane, with cytoplasmic transloca-tion and aggregation detected. GIPC localization was unaltered in neurons and microglia. These results are the ifrst to demonstrate CD93 participation in pathophysiological processes of central nervous system inlfammation.展开更多
Objective To establish a smoke-induced chronic bronchitis rat model and evaluate the patho-logical change semi-quantitatively, and study the characteristics of the inflammatory cells in the bronchoalveolar lav-age flu...Objective To establish a smoke-induced chronic bronchitis rat model and evaluate the patho-logical change semi-quantitatively, and study the characteristics of the inflammatory cells in the bronchoalveolar lav-age fluid (BALF) in various stages. Methods Chronic bronchitis sequential rat model was established by passively inhaling smoke mixture. Experiments were performed in 30 young male Sprague-Dawley rats, which comprised 5 groups in random, i.e.,4 chronic bronchitis model groups and 1 control group. After stained with hematoxylin and eosin, the specimens were studied by semi-quantitative method to evaluate the morphologic changes in various stages. Meanwhile, the inflammatory cells of the BALF and the activity of myeloperoxidase (MPO) of lung tissue were analysed. Results During the process of the chronic bronchitis, the pathologic score was increasing as time went on, and the typical morphologic changes of chronic bronchitis emerged in the group 7 weeks. The total number of inflammatory cells in BALF was increasing as time went on, correlated with the pathologic scores (P <0.01). And the percentage of lymphocyte increased as well as positively correlated with pathologic scores (P < 0. 05) , whereas that of macrophage decreased and negatively correlated with pathologic scores (P <0. 05). The MPO lever of lung tissue was correlated with the pathologic scores (P < 0. 01). But the percentage of the neutrophil in the BALF was just in a high level during the first week, then it maintained relatively lower. Conclusion Smoke-induced chronic bronchitis is a slowly progressive inflammation process. The model we established is convenient and simple for the longitudinal study on the inflammatory process of chronic bronchitis and the therapy in the early stage. The semi-quantitative evaluation for the pathological change is with much more value. During the inflammatory sequential process of early stage of chronic bronchitis, the cellular characteristics are similar to that of the common chronic inflammation.展开更多
This study was designed to investigate the anti-inflammatory effects of volatile oil of Platycladus orientalis(L.)Franco leaves(VOPF)and the underlying molecular mechanisms by using the non-infectious inflammation rat...This study was designed to investigate the anti-inflammatory effects of volatile oil of Platycladus orientalis(L.)Franco leaves(VOPF)and the underlying molecular mechanisms by using the non-infectious inflammation rat models and infectious inflammation mouse models.Ear swelling and intraperitoneal capillary permeability in mice,and carrageenan-induced toe swelling and cotton ball-induced granuloma in rats were used to reveal anti-inflammatory effects of VOPF.Moreover,the lipopolysaccharide(LPS)-induced mouse model of acute lung injury was used to explore the anti-inflammatory mechanism of VOPF.The results showed that VOPF could significantly inhibit auricular swelling,intraperitoneal capillary permeability in mice,and reduce granuloma swelling and paw swelling in rats.Furthermore,it significantly alleviated the pathological damage of the lung tissue.In addition,VOPF could reduce the contents of IL-1β and TNF-αand increase the content of IL-10 in the serum.It had little effect on the expression of p65 but reduced the phosphorylation level of p65 and IκB in NF-κB pathway.In conclusion,VOPF has anti-inflammatory effects and the mechanisms involve the down-regulation of the phosphorylation levels of p65 and IκB and blockage of the NF-κB signaling pathway.展开更多
基金Natural science foundation of Hebei Province(H2020405298)。
文摘OBJECTIVE To establish an in vitro inflammatory model of BV2 by observing the activity,the release amount of NO and the expression of inflammatory factors of microglial cells(BV2)induced by lipopolysaccharides(LPS).METHODS BV2 was routinely cultured in vitro.Cell viability was measured by CCK-8 meth⁃od.And by drew cell growth curve to determine the logarithmic growth cycle of the cells.After 24 h of routine culture,BV2 were induced by adding different concentrations of LPS(0.1,1.0 and 10.0 mg·L-1)for 4,8,12,24 and 48 h,respectively.Meanwhile,the morphological changes of BV2 were observed under inverted microscope to compare the activation degree of microglia at dif⁃ferent time and concentration.Cell activity and nitric oxide(NO)level were determined by CCK-8 and Griess method respectively,which could help to determine the optimal concentration and time of modeling.Finally,It were determined by ELISA that the concentrations of tumor necrosis factorα(TNF-α),interleukin-6(IL-6)and IL-1βin supernatant of LPS 1 mg·L-1 culture for 24 h.RESULTS BV2 were in logarithmic growth phase for 1 to 3 d after subculture.LPS 1 mg·L-1 induced BV2 for 24 or 48 h which could increase the release amount of NO significantly(P<0.05).In order to save time,LPS induced BV2 for 24 h were selected for subsequent experiments.Microglial cells in resting state were observed to be elongated spindle shape under inverted micro⁃scope.After LPS activation,the cell body became larger and the branching processes shrank back,presenting an amoeba-like appearance.ELISA results showed that the concentrations of TNF-α,IL-6 and IL-1βin supernatant of LPS 1 mg·L-1 cultured for 24 h were significantly increased which compared with the control group(P<0.05).CONCLUSION LPS could induce the activation of BV2 and up-regulate the level of inflammatory factors.The optimal condition for establishing stable BV2 microglial inflammatory model was used LPS 1 g·L-1 induced for 24 h.
文摘Using inducers to induce cells to produce inflammatory response is a common in vitro experimental method to study inflammation.However,there are relatively few inflammatory models developed for the cosmetic industry,and there are also great differences in the control of model induction,the selection of inflammatory indicators,and the concentration of inducers.Therefore,in this paper,by systematically studying the effects of Lipopolysaccharide(LPS)on the cell viability,the levels of IL-1α,IL-8 and ROS of human primary keratinocytes,a skin inflammation model based human primary keratinocyte was developed.The results showed that 0.01~100μg/mL LPS had no significant effect on the cell viability of human primary keratinocytes,while 100μg/mL LPS could simultaneously induce human primary keratinocytes to produce large amounts of IL-1αand IL-8,and 0.01μg/mL LPS could induce plentiful ROS.Therefore,a skin inflammation model for differential induction of different inflammatory indicators was established,and the sample OSM2021041301 was tested with this model,it was found that sample OSM2021041301 could significantly inhibit LPS-induced elevated IL-1αand IL-8 levels,the inhibitory effect on LPS-induced elevated ROS level was weak.The results indicated that OSM2021041301 has certain anti-inflammatory effect on inflammation caused by the increase of IL-1α,IL-8 and ROS induced by LPS and its analogues.
基金supported by grants from the National Natural Science Foundation of China (grant number 81625005 to Z.F.)High-level Talents of the Beijing Health System (grant number 2014-3-080 to F.Z.)the program for Beijing Science and Technology of Chinese Medicine (grant number JJ2013-11 to F.Z.)
文摘Periodontitis is an inflammatory autoimmune disease. Treatment should alleviate inflammation, regulate the immune reaction and promote periodontal tissue regeneration. Icariin is the main active ingredient of Epimedii Folium, and it is a promising compound for the enhancement of mesenchymal stem cell function, promotion of bone formation, inhibition of bone resorption, alleviation of inflammation and regulation of immunity. The study investigated the effect of icariin on periodontal tissue regeneration in a minipig model of periodontitis. The minipig model of periodontitis was established. Icariin was injected locally. The periodontal clinical assessment index, a computed tomography(CT) scan, histopathology and enzyme-linked immune sorbent assay(ELISA)were used to evaluate the effects of icariin. Quantitative analysis results 12 weeks post-injection demonstrated that probing depth,gingival recession, attachment loss and alveolar bone regeneration values were(3.72 ± 1.18) mm vs.(6.56 ± 1.47) mm,(1.67 ± 0.59)mm vs.(2.38 ± 0.61) mm,(5.56 ± 1.29) mm vs.(8.61 ± 1.72) mm, and(25.65 ± 5.13) mm3 vs.(9.48 ± 1.78) mm3 in the icariin group and0.9% NaCl group, respectively. The clinical assessment, CT scan, and histopathology results demonstrated significant enhancement of periodontal tissue regeneration in the icariin group compared to the 0.9% NaCl group. The ELISA results suggested that the concentration of interleukin-1 beta(IL-1β) in the icariin group was downregulated compared to the 0.9% NaCl group, which indicates that local injection of icariin relieved local inflammation in a minipig model of periodontitis. Local injection of icariin promoted periodontal tissue regeneration and exerted anti-inflammatory and immunomodulatory function. These results support the application of icariin for the clinical treatment of periodontitis.
基金supported by Medical Key Talents Foundation of Jiangsu Province,China(No:904-KJXW18)by National Natural Science Youth Foundation of China(No.81300227 and No.81300159)
文摘Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea（OSA）.We used a well-described OSA rat model induced with simultaneous intermittent hypoxia.Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled.The rats were exposed to intermittent hypoxia 8 hours daily for 5weeks.The changes of cardiac structure and function were examined by ultrasound.The cardiac pathology,apoptosis,and fibrosis were analyzed by H＆E staining,TUNNEL assay,and picosirius staining,respectively.The expression of inflammation and fibrosis marker genes was analyzed by quantitative real-time PCR and Western blot.Chronic intermittent hypoxia/low pressure resulted in significant increase of left ventricular internal diameters（LVIDs）,endsystolic volume（ESV）,end-diastolic volume（EDV）,and blood lactate level and marked reduction in ejection fraction and fractional shortening.Chronic intermittent hypoxia increased TUNNEL-positive myocytes,disrupted normal arrangement of cardiac fibers,and increased Sirius stained collagen fibers.The expression levels of hypoxia induced factor（HIF）-l α,NF-κB,IL-6,and matrix metallopeptidase 2（MMP-2） were significantly increased in the heart of rats exposed to chronic intermittent hypoxia.In conclusion,the left ventricular function was adversely affected by chronic intermittent hypoxia,which is associated with increased expression of HIF-lα and NF-κB signaling molecules and development of cardiac inflammation,apoptosis and fibrosis.
文摘In order to investigate the effects of interleukin-18 （IL-18） on airway inflammation and the Th1/Th2 cytokine balance in guinea pig asthmatic model as well as its possible mechanisms, the asthmatic model was established by intraperitoneal injection of ovalbumin （OVA） and aerosol challenges into guinea pigs, and 30 treated animals were randomly divided into three groups of 10 animals in each groups, in which group A served as the asthmatic model, group B as the controls and group C as the group treated with IL-18. The counting and categorization of the inflammatory cells in bronchoalveolar lavage fluid （BALF） were performed by using light microscopy, and the contents of cytokines （ IFN-γ, IL- 2, IL-4 and IL-5） were assayed by means of the ELISA kit. The experimental results showed that the numbers of eosinophils （ESO） in BALF of group A, B and C were （97.70 ± 58.03） × 10^6/L, （11.68 × 9.95） × 10^6/L and （28.62 ± 10.46） × 10^6/L, respectively, in which the number of eosinophils in group A was significantly higher than those of group B and C. Also, the number of neutrophils in BALF of group A was even higher than those in group B and C. In addition, the contents of IFN-7 and IL-2 in group A were lower than those in group B and C, but the contents of IL-4 as well as IL-5 were rather higher than those in group B and C. It is evident from the above observations that IL-18 can effectively inhibit the asthmatic inflammatory cells in BALF with an imbalance of the Thl/Th2 cytokines, thus offer- ing the experimental basis for the clinical application of IL-18 in the prevention and treatment of asthma.
基金supported by the National Natural Science Foundation of China,No.31170766the Nantong Municipal Social Undertakings Technological Innovation and Demonstration Project Foundation,No.HS2012032the Natural Science Pre-research Project Foundation of Nantong University in 2012,No.12ZY020
文摘CD93 and GAIP-interacting protein, C termius （GIPC） have been shown to interactively alter phagocytic processes of immune cells. CD93 and GIPC expression and localization during cen-tral nervous system inflammation have not yet been reported. In this study, we established a rat model of brain inlfammation by lipopolysaccharide injection to the lateral ventricle. In the brain of rats with inlfammation, western blots showed increased CD93 expression that decreased over time. GIPC expression was unaltered. Immunohistochemistry demonstrated extensive distribution of CD93 expression mainly in cell membranes in the cerebral cortex. After lipopoly-saccharide stimulation, CD93 expression increased and then reduced, with distinct staining in the cytoplasm and nucleus. Double immunolfuorescence staining in cerebral cortex of normal rats showed that CD93 and GIPC widely expressed in resting microglia and neurons. CD93 was mainly expressed in microglial and neuronal cell membranes, while GIPC was expressed in both cell membrane and cytoplasm. In the cerebral cortex at 9 hours after model establishment, CD93-immunoreactive signal diminished in microglial membrane, with cytoplasmic transloca-tion and aggregation detected. GIPC localization was unaltered in neurons and microglia. These results are the ifrst to demonstrate CD93 participation in pathophysiological processes of central nervous system inlfammation.
基金Supported by the fund from Shanghai Science and Technology Committee (004119060)
文摘Objective To establish a smoke-induced chronic bronchitis rat model and evaluate the patho-logical change semi-quantitatively, and study the characteristics of the inflammatory cells in the bronchoalveolar lav-age fluid (BALF) in various stages. Methods Chronic bronchitis sequential rat model was established by passively inhaling smoke mixture. Experiments were performed in 30 young male Sprague-Dawley rats, which comprised 5 groups in random, i.e.,4 chronic bronchitis model groups and 1 control group. After stained with hematoxylin and eosin, the specimens were studied by semi-quantitative method to evaluate the morphologic changes in various stages. Meanwhile, the inflammatory cells of the BALF and the activity of myeloperoxidase (MPO) of lung tissue were analysed. Results During the process of the chronic bronchitis, the pathologic score was increasing as time went on, and the typical morphologic changes of chronic bronchitis emerged in the group 7 weeks. The total number of inflammatory cells in BALF was increasing as time went on, correlated with the pathologic scores (P <0.01). And the percentage of lymphocyte increased as well as positively correlated with pathologic scores (P < 0. 05) , whereas that of macrophage decreased and negatively correlated with pathologic scores (P <0. 05). The MPO lever of lung tissue was correlated with the pathologic scores (P < 0. 01). But the percentage of the neutrophil in the BALF was just in a high level during the first week, then it maintained relatively lower. Conclusion Smoke-induced chronic bronchitis is a slowly progressive inflammation process. The model we established is convenient and simple for the longitudinal study on the inflammatory process of chronic bronchitis and the therapy in the early stage. The semi-quantitative evaluation for the pathological change is with much more value. During the inflammatory sequential process of early stage of chronic bronchitis, the cellular characteristics are similar to that of the common chronic inflammation.
基金the National Natural Science Foundation of China(No.31200264)the Fundamental Research Funds for Central Universities(South-Central University for NationalitiesNo.CZY19028,No.CZY20048).
文摘This study was designed to investigate the anti-inflammatory effects of volatile oil of Platycladus orientalis(L.)Franco leaves(VOPF)and the underlying molecular mechanisms by using the non-infectious inflammation rat models and infectious inflammation mouse models.Ear swelling and intraperitoneal capillary permeability in mice,and carrageenan-induced toe swelling and cotton ball-induced granuloma in rats were used to reveal anti-inflammatory effects of VOPF.Moreover,the lipopolysaccharide(LPS)-induced mouse model of acute lung injury was used to explore the anti-inflammatory mechanism of VOPF.The results showed that VOPF could significantly inhibit auricular swelling,intraperitoneal capillary permeability in mice,and reduce granuloma swelling and paw swelling in rats.Furthermore,it significantly alleviated the pathological damage of the lung tissue.In addition,VOPF could reduce the contents of IL-1β and TNF-αand increase the content of IL-10 in the serum.It had little effect on the expression of p65 but reduced the phosphorylation level of p65 and IκB in NF-κB pathway.In conclusion,VOPF has anti-inflammatory effects and the mechanisms involve the down-regulation of the phosphorylation levels of p65 and IκB and blockage of the NF-κB signaling pathway.
