The gut microbiota is regarded as the "eighth organ" of the human body and plays a critical regulatory role in the occurrence and progression of various diseases. Ulcerative colitis （UC） is a chronic inflammatory bowel disease with a complex etiology and a tendency toward recurrent episodes. In recent years， studies have shown that gut microbiota dysbiosis plays a key role in its pathological processes. Meanwhile， an increasing number of studies have demonstrated that imbalances in the gut microbiota and abnormalities in its metabolites are closely associated with the development of atrial fibrillation （AF）. Although UC and AF belong to diseases of the digestive system and cardiovascular system， respectively， both exhibit systemic inflammatory characteristics and are often accompanied by gut microbiota dysregulation and abnormal metabolic products. However， systematic investigations into the mechanisms by which gut microbiota-derived metabolites act in these two diseases remain limited. Based on this， the present study adopts literature review and theoretical analysis methods， taking the "gut microbiota-gut-heart" axis as the entry point， to systematically summarize the signaling networks of three key classes of metabolites， i.e.， short-chain fatty acids （SCFAs）， bile acids （BAs）， and trimethylamine N-oxide （TMAO）， in the comorbidity mechanism of UC and AF. The findings indicate that these metabolites may activate key inflammatory pathways， such as NF-κB and NLRP3， thereby synergistically mediating intestinal barrier dysfunction and systemic inflammation and constructing a potential comorbidity network. On this basis， potential intervention strategies for the treatment of UC-AF comorbidity， including probiotic intervention and fecal microbiota transplantation， are further discussed. This study aims to provide new theoretical evidence and research perspectives for prevention and treatment strategies of cross-system diseases.

Based on the holistic view of "spleen-vessels-heart-spirit" system， this article explores the pathogenesis and progression of atrial fibrillation. It is proposed that the onset of atrial fibrillation is due to failure of the spleen to transport and disharmony of blood vessels； phlegm and blood stasis obstructing the collaterals and damage to the heart structure are the basis of its pathogenesis； the unclear mind and disorder of body and spirit are the causes of its progression. Based on the characteristics of pathological changes in different stages of the disease， it is proposed that early treatment should focus on restoring the middle jiao， clearing and promoting blood vessels， using modified Yigong Powder （异功散）； during the progression of the disease， treatment should remove blood stasis and phlegm， nourish heart and protect the pulse， using self-prescribed modified Mengshi Tongmai Decoction （礞石通脉汤）； meanwhile， calming mind and stabilizing palpitations， and regulating spirit should be sequentially incorporated， with self-prescribed Jiazao Ningmai Decoction （甲枣宁脉汤） or Shenying Dingji Decoction （参英定悸汤） and modified as appropriate. Clinical treatment should focus on the whole disease course of atrial fibrillation， implementing stage-based treatments to enable early intervention and holistic regulation.

Paroxysmal atrial fibrillation can be attributed to the category of xinji （palpitations） and zhangchong （severe palpitations） in traditional Chinese medicine， and its onset has the characteristics of urgency， change， and movement， which is similar to the characteristics of diseases induced by wind pathogen. It is believed that the internal movement of wind pathogen runs through the whole course of this disease， and palpitations due to wind as the direct pathogenesis. Palpitations caused by wind pathogen showed different characteristics of deficiency and excess pattern. In the acute exacerbation period， excess wind is the main cause of disease. For excessive heat generating wind， the treatment is to clear the liver and extinguish wind by self-modified Lingxia Qinggan Decoction （羚夏清肝汤）； for blood stasis generating wind， the treatment is to remove blood stasis and stop wind by self-modified Yandan Limai Decoction （延丹理脉汤）； for phlegm-heat accumulation with wind， the treatment is to dissolve phlegm and eliminate wind by self-modified Lianlou Danxing Decoction （连蒌胆星汤）. In the prolonged recovery period， deficiency wind is more common. For stirring of wind due to yin deficiency， the treatment is to nourish yin and extinguish wind by self-modified Zaoshao Zhenzhu Deoction （枣芍珍珠汤）； for spleen deficiency generating wind， the treatment is to strengthen spleen and nourish wind by self-modified Shenying Dingji Deoction （参英定悸汤）. Clinical prescriptions closely follow the characteristics of wind， weigh the changes of deficiency and excess， tailor with the patterns， and regulate qi and blood of the zang-fu organs， in order to extinguish wind and arrest convulsion.

AIM:To investigate the effect of Huangqi-Danggui decoction(HQDG)on the brain tissue of rats with cerebral ischemia/reperfusion(I/R)injury for 7 d by regulating macroautophagy and chaperone-mediated autophagy(CMA),and to explore its mechanism.METHODS:Male SD rats were randomly divided into sham group,model group,HQDG group and Xuesaitong(XST)group.Determination of main chemical components of HQDG by liquid chro-matography-mass spectrometry.The model of middle cerebral artery occlusion/reperfusion in rats was established by the left modified thread embolism method,and the changes of cerebral blood flow were observed by laser speckle blood flow imager.Zea Longa score was used to observe the neurological deficit.HE staining was used to observe the degree of nerve cell injury.The changes of neurovascular unit and autophagosomes in brain tissue were observed by transmission electron microscopy.Immunohistochemical method was used to detect the expression of LC3,P62,lysosome-associated membrane protein-2A(LAMP-2A),heat shock protein 70(HSP70)and myocyte enhancer factor 2D(MEF2D)proteins.Western blot was used to detect the expression of autophagy-related proteins P62 and LC3-Ⅱ/LC3-I.RESULTS:Compared with the sham group,the neurological deficit score in model group was significantly higher(P<0.01).A large number of nerve cells showed necrosis and nuclear dissolution,with the cell arrangement being disordered.The number of autophagosomes increased.The protein expression levels of LC3,LAMP-2A,HSP70 and MEF2D in brain tissue increased,while the ex-pression level of P62 protein decreased(P<0.05 or P<0.01).Compared with the model group,the scores of neurological deficit in brain tissue in HQDG and XST groups were significantly lower(P<0.01).Cell damage was significantly re-duced.The number of autophagosomes further increased.The expression levels of LAMP-2A,HSP70,MEF2D and P62 proteins in brain tissue decreased,while the expression levels of LC3-Ⅱ/LC3-I protein increased(P<0.05 or P<0.01).CONCLUSION:HQDG can alleviate cerebral ischemia/reperfusion injury in rats and exert neuroprotective effects by ac-tivating macroautophagy and reducing CMA.

Obstructive sleep apnea （OSA） is a sleep disorder with a slow course and is often accompanied by multiple serious complications， having highly consistent pathogenic characteristics with the latent pathogen. By exploreing its pathogenesis and treatment based on the latent pathogen theory in traditional Chinese medicine， it is believed that congenital healthy qi deficiency is the root， while internal latent phlegm and stasis is the branch， and external pathogenic seven emotions are causing factors. In terms of treatment， it is necessary to target at root deficiency and use nourishing medicinals according to depletion degree of lungs， spleen， and kidneys. When protecting the healthy qi， it is important to prevent the generation and inducing of latent pathogen. Simultaneously， it is also critical to put focus on phlegm stasis by clearing existing latent pathogens with medicinals having the function of dissolving phlegm and dispelling stasis， as well as regulating liver and lung qi. All these are expected to provide new ideas and methods for the treatment of OSA patients in clinical practice.