BACKGROUND:Troxerutin has been found to have a significant ameliorative effect on brain disorders,but there are fewer studies on the effects of troxerutin on the treatment of cerebral infarction and on neuronal cells. OBJECTIVE:To investigate the mechanism by which troxerutin regulates nuclear factor-κB signaling pathway to reduce brain injury and neuronal apoptosis in cerebral infarction rats. METHODS:Fifty clean grade rats were randomized into healthy group,model group,and troxerutin+nuclear factor-κB agonist group,troxerutin group,and nuclear factor-κB inhibitor group.Except for the healthy group,all other groups were used to establish a rat model of cerebral infarction by arterial ligation.The healthy and model groups were treated once a day with an equal amount of physiological saline by gavage.The troxerutin+nuclear factor-κB agonist group was intervened with 72 mg/kg troxerutin by gavage+20 mg/kg RANK intraperitoneally.The troxerutin group was treated with 72 mg/kg troxerutin by gavage.The nuclear factor κB inhibitor group was intervened intraperitoneally with 120 mg/kg nuclear factor κB inhibitor pyrrolidine disulfiram.Administration in each group was given once a day for 30 continuous days.Zea-longa was used to detect neurological damage in rats,hematoxylin-eosin staining was used to observe pathological changes,TUNEL was used to detect neuronal apoptosis,and immunoblotting and PCR were used to detect the expression of nuclear factor-κB p65 and nuclear factor-κB p50 at protein and mRNA levels,respectively. RESULTS AND CONCLUSION:Compared with the healthy group,the neurological function score,neuronal apoptosis rate,nuclear factor-κB p65,nuclear factor-κB p50 mRNA and protein expression levels were elevated in the model group(P＜0.05).Compared with the model group,the neurological function score,neuronal apoptosis rate,nuclear factor-κB p65 and nuclear factor-κB p50 mRNA and protein expression levels were decreased in the troxerutin+nuclear factor-κB agonist group(P＜0.05).Compared with the troxerutin+nuclear factor-κB agonist group,the neurological function score,neuronal apoptosis rate,nuclear factor-κB p65 and nuclear factor-κB p50 mRNA and protein expression levels were reduced in the troxerutin group and nuclear factor-κB inhibitor group(P＜0.05).In addition,there was no difference between the troxerutin group and the nuclear factor-κB inhibitor group(P＞0.05).In the model group,there was a large number of cytoplasmic vacuolation,obvious edema and necrosis,and a large number of inflammatory cell infiltrations.In the troxerutin+nuclear factor-κB agonist,the swelling of brain tissue was reduced,and reticulate structures and condensed cells were reduced,still with some edema.In the troxerutin group and nuclear factor-κB inhibitor group,brain tissue swelling,neuronal edema degeneration,cytoplasmic vacuolation and neuronal nucleus consolidation were reduced,and the inflammatory cell infiltration was significantly decreased.To conclude,troxrutin can reduce the expression of neurological impairment,inhibit neuronal apoptosis and improve the pathological injury of brain tissue in rats with cerebral infarction,and its mechanism of action may be related to the modulation of nuclear factor-κB expression and related signaling pathways.

BACKGROUND:Cistanoside A has the effects of anti-inflammation,antioxidation,antioxidation,reducing renal damage and anti-osteoporosis,but its effect on osteoclast differentiation,function and its underlying molecular mechanisms remain unclear. OBJECTIVE:To investigate the effect of Cistanoside A on osteoclast differentiation and bone resorption induced by receptor activator of nuclear factor kappa-B ligand(RANKL)in vitro and its mechanism. METHODS:Bone marrow macrophages were obtained from the femur and tibia of 4-6-week-old C57BL/6 mice.The cytotoxic effect of Cistanoside A(5,10,20,40,80,and 160 μmol/L)on bone marrow macrophage viability was examined using the cell counting kit-8 assay kit.Tartrate-resistant acid phosphatase staining was performed to observe the effect of different concentrations of Cistanoside A on osteoblast differentiation and its effective intervention concentration was determined.There was positive control group,Cistanoside A low,medium,and high dose groups(40,80,and 160 μmol/L).After cell attachment,50 ng/mL RANKL was added to induce osteoblast differentiation,and the corresponding dose of Cistanoside A was added to the Cistanoside A low,medium,and high dose groups,respectively.F-actin ring and 2-(4-Amidinophenyl)-6-indolecarbamidine dihydrochloride staining were performed to detect the effects of Cistanoside A on the formation of osteoclasts.Toluidine blue staining of bone abrasion slices was used to observe the effects of Cistanoside A on bone resorption function of osteoclasts.The expression of upstream and downstream proteins of the JNK/MAPK pathway was detected by Western blot.The expression of genes related to osteoclast differentiation and bone resorption function such as tartrate-resistant acid phosphatase,DC-STAMP,Nfatc-1,Ctsk and c-Fos was detected by RT-qPCR. RESULTS AND CONCLUSION:Tartrate-resistant acid phosphatase staining,F-actin ring staining and resorption pit assay showed that Cistanoside A significantly inhibited RANKL-induced osteoclast differentiation and bone resorption in a dose-dependent manner compared with the positive control group.The results of RT-qPCR showed that compared with the positive control group,both high and low dose groups of Cistanoside A could significantly downregulate the mRNA expression of tartrate-resistant acid phosphatase,DC-STAMP,Nfatc-1,Ctsk and c-Fos in a dose-dependent manner.The results of western blot assay showed that the high dose group of Cistanoside A significantly inhibited the expression of p-JNK protein at 10,20,30 and 60 minutes of intervention;compared with the positive control group,Cistanoside A significantly inhibited the expression of Nfatc1 and c-Fos proteins in a dose-dependent manner.To conclude,Cistanoside A could inhibit the formation and bone resorption of osteoclasts by reducing the level of p-JNK protein,inhibiting the activation of MAPK pathway and the expression of key genes in osteoclasts.

BACKGROUND:Stem cell transplantation is a novel therapy for myocardial infarction,but the extremely hostile microenvironment in the infarct area results in low survival rate of stem cells and little long-term effect.Exercise preconditioning is a way to induce endogenous protective effects through exercise,which can be used as a new strategy for prevention and treatment of cardiac rehabilitation. OBJECTIVE:To evaluate whether exercise preconditioning potentiates the cardioprotective effects of adipose-derived stem cell transplantation following myocardial infarction in rats and to explore the mechanism of angiogenesis. METHODS:Six-week-old male SD rats were randomly divided into control group,modeling group,stem cell group,and stem cell plus exercise group.Acute myocardial infarction model was made by coronary artery occlusion,and sham operation was performed in control group.The stem cell plus exercise group underwent aerobic exercise for 8 weeks before modeling,and adipose-derived stem cell transplantation was performed 30 minutes after modeling.The stem cell group performed only adipose-derived stem cell transplantation.One and seven days after stem cell transplantation,the expression levels of myocardial total Akt(t-Akt),phosphorylated Akt(p-Akt),vascular endothelial growth factor(VEGF),total endothelial nitric oxide synthase(t-eNOS),and phosphorylated endothelial nitric oxide synthase(p-eNOS)protein were measured by western blotting,and the ratios of p-Akt/t-Akt and p-eNOS/t-eNOS were calculated.At 4 weeks after stem cell transplantation,the heart structure and function as well as myocardial blood flow were detected by color Doppler ultrasound diagnostic system.Myocardial infarction area was measured by TTC staining.Myocardial interstitial collagen deposition was examined by Masson staining.Myocardial capillary density was detected by immunofluorescence staining,and myocardial apoptosis was measured by TUNEL staining. RESULTS AND CONCLUSION:(1)Four weeks after stem cell transplantation:Compared with control group,left ventricular shortening fraction,left ventricular ejection fraction,myocardial capillary density,and myocardial blood flow decreased(P<0.05),myocardial infarction area,collagen volume fraction,and apoptosis increased(P<0.05)in the modeling group.Compared with the modeling group,the above indexes(except for left ventricular fractional shortening and left ventricular ejection fraction)in the stem cell group improved(P<0.05).Compared with the stem cell group,the above parameters were further improved in the stem cell plus exercise group(P<0.05).(2)One day after stem cell transplantation:Compared with the control group,the protein expression of t-Akt,p-Akt,VEGF,t-eNOS,p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS had no significant changes in the modeling group(P>0.05).Compared with the modeling group,there were no significant changes in the above indexes in the stem cell group(P>0.05),and p-Akt protein expression and the ratio of p-Akt/t-Akt were up-regulated in the stem cell plus exercise group(P<0.05).(3)Seven days after stem cell transplantation:Compared with the control group,the protein expression of p-Akt,VEGF,p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS were decreased in the modeling group(P<0.05).Compared with the modeling group,there were no significant changes in all parameters in the stem cell group(P>0.05),and the protein expression of p-Akt,VEGF p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS were increased in the stem cell plus exercise group(P<0.05).These findings confirm that exercise preconditioning can potentiate the therapeutic effect of adipose-derived stem cells on cardiac remodeling in rats with myocardial infarction,and its mechanism is associated with the promotion of myocardial angiogenesis and blood perfusion.

Clinical practice guidelines represent the best recommendations for patient care. They are developed through systematically reviewing currently available clinical evidence and weighing the relative benefits and risks of various interventions. However, clinical practice guidelines have to go through a long translation cycle from development and revision to clinical promotion and application, facing problems such as scattered distribution, high duplication rate, and low actual utilization. At present, the clinical practice guideline information platform can directly or indirectly solve the problems related to the lengthy revision cycles, decentralized dissemination and limited application of clinical practice guidelines. Therefore, this paper systematically examines different types of clinical practice guideline information platforms and investigates their corresponding challenges and emerging trends in platform design, data integration, and practical implementation, with the aim of clarifying the current status of this field and providing valuable reference for future research on clinical practice guideline information platforms.

ObjectiveTo explore the mechanism of action of Wendantang on ApoE^-/- hyperlipidemic mice using non-targeted metabolomics technology. MethodsMale C57BL/6J mice served as the normal control group （n=6）， and they were fed with regular chow， while male ApoE^-/- mice constituted the high-fat group （n=30）， and they were fed with a 60% high-fat diet. After 11 weeks of model establishment， the mice in the high-fat group were randomly divided into the model group， simvastatin group （3.3 mg·kg^-1）， and high-dose， medium-dose， and low-dose groups of Wendantang （26， 13， 6.5 g·kg^-1， respectively， in terms of crude drug amount）， with six mice in each group. The normal control group and the model group were gavaged with an equivalent volume of normal saline， and all groups continued to be fed their respective diets， receiving daily medication for 10 weeks with weekly body weight measurements. Serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， low-density lipoprotein cholesterol （LDL-C）， free fatty acids （NEFA）， blood glucose （GLU）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） were detected in the mice. Pathological changes in liver tissue were observed using hematoxylin-eosin （HE） staining， and ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry （UPLC-Q-TOF-MS/MS） was employed for metabolomic analysis of mouse liver tissue. ResultsCompared to the normal control group， the model group exhibited significantly increased body weight， blood lipid levels， and liver function （P<0.05， P<0.01）， with disordered liver tissue structure， swollen hepatocytes， and accompanying vacuolar fatty degeneration and inflammatory cell infiltration. Compared to the model group， the simvastatin group and Wendantang groups showed significantly reduced body weight， TG， NEFA， GLU， ALT， and AST levels （P<0.05， P<0.01）， with a significant increase in HDL-C levels （P<0.05， P<0.01）， demonstrating a dose-dependent effect. The lesion of the liver tissue section was obviously improved after administration， tending towards a normal liver tissue morphology. Analysis of liver metabolites revealed 86 differential metabolites between the normal control group and the model group， with the high-dose group of Wendantang able to regulate 56 of these metabolites. Twenty-two differential metabolites associated with hyperlipidemia were identified， mainly including chenodeoxycholic acid， hyocholic acid， taurine， glycocholic acid， dihydroceramide， hydroxy sphingomyelin C14∶1， arachidonic acid， and linoleic acid， enriching 22 metabolic pathways， with 4 being the most significant （P<0.05）， namely primary bile acid biosynthesis， sphingolipid metabolism， unsaturated fatty acid biosynthesis， and linoleic acid metabolism pathways. ConclusionWendantang can improve blood lipid levels and liver function in ApoE^-/- hyperlipidemic mice， which may be related to the regulation of primary bile acid biosynthesis， sphingolipid metabolism， unsaturated fatty acid biosynthesis， and linoleic acid metabolism pathways.

ObjectiveTo explore the effects of compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata on the expression of type 2 innate lymphoid cells（ILC2s）-related factors in the lung of allergic rhinitis（AR）mice. MethodsAccording to the random number table method，fifty-four C57BL/6J mice were randomly divided into the following groups： Blank group，model group，Mahuang Fuzi Xixintang group，Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba and Asari Radix et Rhizoma group，Ephedrae Herba and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba group，Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group （6 mice in each group）. Except the blank group，the other groups were subjected to intraperitoneal injection of ovalbumin（OVA）and intranasal challenge to induce AR. After the AR model was established，the mice in the blank group and the model group were given 0.2 mL·d^-1 normal saline by gavage，while those in the Mahuang Fuzi Xixintang group（2.31 g·kg^-1），Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group（1.54 g·kg^-1）， Ephedrae Herba and Asari Radix et Rhizoma group（1.16 g·kg^-1）， Ephedrae Herba and Aconiti Lateralis Radix Praeparata group（1.93 g·kg^-1），Ephedrae Herba group（0.77 g·kg^-1），Aconiti Lateralis Radix Praeparata group（1.16 g·kg^-1），and Asari Radix et Rhizoma group（0.39 g·kg^-1）were given corresponding medicine by gavage，with the treatment lasting for 14 consecutive days. The survival state of mice in each group was observed， and the levels of serum immunoglobulins E（IgE）after intranasal challenge were measured by enzyme-linked immunosorbent assay（ELISA）. The pathological changes of nasal and lung tissues were observed by hematoxylin-eosin（HE）staining. The expression of ILC2s in lung tissue of mice was detected by immunofluorescence（IF）. The mRNA expression of GATA binding protein 3（GATA3），retinoic acid receptor-related orphan receptor-α（RORα）， and inhibitor of DNA binding 2（ID2）in the lung tissue of mice was detected by quantitative real-time polymerase chain reaction（real-time PCR）. The levels of IgE，interleukin（IL）-4，IL-5， and IL-13 in serum were detected by ELISA. ResultsCompared with the blank group，the model group had poor survival state of mice and significantly increased serum IgE level after intranasal challenge（p<0.01）. Additionally，the mice in the model group showed a large amount of neutrophil infiltration in the mucosa of the posterior turbinate， obvious nasal mucosal bleeding and purulent secretion，shed epithelium， thickened bronchial wall，obvious intravascular hyperemia and edema，diffusion and infiltration of a large number of inflammatory cells，seriously damaged alveolar structure，and local lung consolidation. The model group also exhibited significantly increased expression of ILC2s in the lung tissue（P<0.01），increased mRNA expression of GATA3 and RORα，decreased mRNA expression of ID2（P<0.05，P<0.01），and increased levels of serum IgE， IL-4，IL-5，and IL-13（P<0.05，P<0.01）. Compared with the model group，the Mahuang Fuzi Xixintang group and the other medicine treatment groups showed improved survival state of mice， significantly reduced inflammatory cell infiltration in the nasal and lung tissues，a small amount of nasal mucosal bleeding，trachea wall thinning，and no hyperemia，edema， and nasal secretions. Furthermore， the expression of ILC2s in lung tissue was significantly decreased（P<0.01）. The mRNA expression level of GATA3 was decreased（P<0.05），especially in the Aconiti Lateralis Radix Praeparata group（P<0.01）. The expression mRNA levels of RORα were decreased only in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group and the Ephedrae Herba group（P<0.05）. The levels of serum IgE were decreased（P<0.05）， and IL-5 levels were significantly decreased（P<0.01）. IL-4 levels were significantly decreased in the groups except the Aconiti Lateralis Radix Praeparata group（P<0.01），and the level of IL-13 in the Mahuang Fuzi Xixintang group was decreased（P<0.05）. The levels of IL-13 in were significantly decreased in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group， Ephedrae Herba group， Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group（P<0.01）. ConclusionDifferent compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata can reduce the inflammation of OVA-induced AR mice and has more advantages in reducing the secretion of IgE and IL-5. The compatibility of Ephedrae Herba and Aconiti Lateralis Radix Praeparata has the most advantage in reducing the mRNA expression of GATA3 and RORα to inhibit the expression of ILC2s and thus exert the anti-allergic effect，while the other compatibility has the extensive advantage in inhibiting the mRNA expression of GATA3.

With the main pathological features of glomerulosclerosis and interstitial fibrosis， renal fibrosis is a key pathological process causing chronic kidney disease to progress to end-stage disease. As a cellular autophagic process， mitochondrial autophagy plays a crucial role in maintaining mitochondrial mass and functional stability. Mitochondrial dysfunction is considered to be one of the key factors driving the progression of fibrosis. Phosphatase and tension protein homologue （PTEN） induce various signalling pathways such as putative kinase 1/parkin， Nip3-like protein X/Bcl-2 interacting protein 3， and FUN14 structural domain-containing protein 1 to activate mitochondrial autophagy to participate in the regulation of fibrogenic factors， amelioration of oxidative stress， and inhibition of inflammatory response and apoptosis， which in turn effectively slows down the progression of renal fibrosis. Studies have shown that traditional Chinese medicine monomers and compound preparations， including phenolics， terpenoids， ketones， and alkaloids， can regulate mitochondrial autophagy-related signalling pathways and achieve significant clinical efficacy in intervening in the progression of renal fibrosis for the treatment of chronic kidney disease. This paper summarized the mechanism of mitochondrial autophagy and the research progress of traditional Chinese medicine intervention in renal fibrosis to provide new ideas for the study of the mechanism of traditional Chinese medicine in treating renal fibrosis.

This paper summarizes Professor AI Rudi's experience in the diagnosis and treatment of skin pruritus based on the "unity of restoring form， regulating qi， and harmonizing spirit"， employing internal herbal medicine combined with external treatments. It is believed that the core pathogenesis of pruritus is the "imbalance of form， qi， and spirit"， with disturbed spirit as the onset， disordered qi as the key pathogenic factor， and physical changes as the manifestation of the disease. The treatment principle follows "restoring form-regulating qi-harmonizing spirit"， with a combination of internal and external therapies， and differentiation based on deficiency and excess. For excess conditions caused by pathogenic disturbances to the heart spirit， treatment is based on different patterns of wind-heat， damp-heat， and blood-heat， using Sangye （Morus alba）-Sangbaipi （Morus alba cortex）-Longchi （Draconis os） to disperse wind and clear heat， calm the spirit； Difuzi （Kochia scoparia）-Qinghao （Artemisia annua）-Tanxiang （Santalum album） to clear damp-heat and aromatically open the spirit； Mudanpi （Paeonia suffruticosa）-Chuanxiong （Ligusticum chuanxiong）-Shuiniujiao （Bubalus bubalis cornua） to cool the blood， activate circulation， and calm the spirit. For deficiency conditions caused by insufficient nourishment of the heart spirit， treatment is based on patterns of qi deficiency or blood deficiency， using Huangqi （Astragalus membranaceus）-Fuping （Lemna minor）-Wuweizi （Schisandra chinensis） to tonify the qi and stabilize the exterior； Heshouwu （Polygonum multiflorum）-Jili （Tribulus terrestris）-Shouwuteng （Polygonum multiflorum vine） to nourish the blood， moisten dryness， and calm the spirit. External treatments integrate traditional Chinese medicine therapies such as medicinal baths， gua sha， and ear acupuncture， with custom herbal wash formulas for restoring form， jojoba oil gua sha for regulating qi， and ear seed therapy using Wangbuliuxing （Vaccaria segetalis） for harmonizing the spirit， achieving a holistic treatment effect for form， qi， and spirit.

ObjectiveTo explore the effects of compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata on the expression of type 2 innate lymphoid cells（ILC2s）-related factors in the lung of allergic rhinitis（AR）mice. MethodsAccording to the random number table method，fifty-four C57BL/6J mice were randomly divided into the following groups： Blank group，model group，Mahuang Fuzi Xixintang group，Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba and Asari Radix et Rhizoma group，Ephedrae Herba and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba group，Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group （6 mice in each group）. Except the blank group，the other groups were subjected to intraperitoneal injection of ovalbumin（OVA）and intranasal challenge to induce AR. After the AR model was established，the mice in the blank group and the model group were given 0.2 mL·d^-1 normal saline by gavage，while those in the Mahuang Fuzi Xixintang group（2.31 g·kg^-1），Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group（1.54 g·kg^-1）， Ephedrae Herba and Asari Radix et Rhizoma group（1.16 g·kg^-1）， Ephedrae Herba and Aconiti Lateralis Radix Praeparata group（1.93 g·kg^-1），Ephedrae Herba group（0.77 g·kg^-1），Aconiti Lateralis Radix Praeparata group（1.16 g·kg^-1），and Asari Radix et Rhizoma group（0.39 g·kg^-1）were given corresponding medicine by gavage，with the treatment lasting for 14 consecutive days. The survival state of mice in each group was observed， and the levels of serum immunoglobulins E（IgE）after intranasal challenge were measured by enzyme-linked immunosorbent assay（ELISA）. The pathological changes of nasal and lung tissues were observed by hematoxylin-eosin（HE）staining. The expression of ILC2s in lung tissue of mice was detected by immunofluorescence（IF）. The mRNA expression of GATA binding protein 3（GATA3），retinoic acid receptor-related orphan receptor-α（RORα）， and inhibitor of DNA binding 2（ID2）in the lung tissue of mice was detected by quantitative real-time polymerase chain reaction（real-time PCR）. The levels of IgE，interleukin（IL）-4，IL-5， and IL-13 in serum were detected by ELISA. ResultsCompared with the blank group，the model group had poor survival state of mice and significantly increased serum IgE level after intranasal challenge（p<0.01）. Additionally，the mice in the model group showed a large amount of neutrophil infiltration in the mucosa of the posterior turbinate， obvious nasal mucosal bleeding and purulent secretion，shed epithelium， thickened bronchial wall，obvious intravascular hyperemia and edema，diffusion and infiltration of a large number of inflammatory cells，seriously damaged alveolar structure，and local lung consolidation. The model group also exhibited significantly increased expression of ILC2s in the lung tissue（P<0.01），increased mRNA expression of GATA3 and RORα，decreased mRNA expression of ID2（P<0.05，P<0.01），and increased levels of serum IgE， IL-4，IL-5，and IL-13（P<0.05，P<0.01）. Compared with the model group，the Mahuang Fuzi Xixintang group and the other medicine treatment groups showed improved survival state of mice， significantly reduced inflammatory cell infiltration in the nasal and lung tissues，a small amount of nasal mucosal bleeding，trachea wall thinning，and no hyperemia，edema， and nasal secretions. Furthermore， the expression of ILC2s in lung tissue was significantly decreased（P<0.01）. The mRNA expression level of GATA3 was decreased（P<0.05），especially in the Aconiti Lateralis Radix Praeparata group（P<0.01）. The expression mRNA levels of RORα were decreased only in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group and the Ephedrae Herba group（P<0.05）. The levels of serum IgE were decreased（P<0.05）， and IL-5 levels were significantly decreased（P<0.01）. IL-4 levels were significantly decreased in the groups except the Aconiti Lateralis Radix Praeparata group（P<0.01），and the level of IL-13 in the Mahuang Fuzi Xixintang group was decreased（P<0.05）. The levels of IL-13 in were significantly decreased in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group， Ephedrae Herba group， Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group（P<0.01）. ConclusionDifferent compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata can reduce the inflammation of OVA-induced AR mice and has more advantages in reducing the secretion of IgE and IL-5. The compatibility of Ephedrae Herba and Aconiti Lateralis Radix Praeparata has the most advantage in reducing the mRNA expression of GATA3 and RORα to inhibit the expression of ILC2s and thus exert the anti-allergic effect，while the other compatibility has the extensive advantage in inhibiting the mRNA expression of GATA3.

With the main pathological features of glomerulosclerosis and interstitial fibrosis， renal fibrosis is a key pathological process causing chronic kidney disease to progress to end-stage disease. As a cellular autophagic process， mitochondrial autophagy plays a crucial role in maintaining mitochondrial mass and functional stability. Mitochondrial dysfunction is considered to be one of the key factors driving the progression of fibrosis. Phosphatase and tension protein homologue （PTEN） induce various signalling pathways such as putative kinase 1/parkin， Nip3-like protein X/Bcl-2 interacting protein 3， and FUN14 structural domain-containing protein 1 to activate mitochondrial autophagy to participate in the regulation of fibrogenic factors， amelioration of oxidative stress， and inhibition of inflammatory response and apoptosis， which in turn effectively slows down the progression of renal fibrosis. Studies have shown that traditional Chinese medicine monomers and compound preparations， including phenolics， terpenoids， ketones， and alkaloids， can regulate mitochondrial autophagy-related signalling pathways and achieve significant clinical efficacy in intervening in the progression of renal fibrosis for the treatment of chronic kidney disease. This paper summarized the mechanism of mitochondrial autophagy and the research progress of traditional Chinese medicine intervention in renal fibrosis to provide new ideas for the study of the mechanism of traditional Chinese medicine in treating renal fibrosis.