ObjectiveTo investigate the effect of Niuhuang Qingxinwan （NHQXW） in improving intracerebral hemorrhage （ICH） with Tanre Fushi （phlegm-heat and fu-organ excess） syndrome by maintaining blood-brain barrier （BBB） integrity， and to explore its potential mechanism. MethodsMale mice were administered with 15% autologous feces for 3 consecutive days to simulate spontaneous Tanre Fushi syndrome， followed by surgical induction of collagenase-induced ICH on the fourth day. Mice were randomly assigned to seven groups： Sham， Sham+NHQXW-H， collagenase， collagenase+feces， and NHQXW intervention groups at low （NHQXW-L， 0.225 g·kg^-1）， medium （NHQXW-M， 0.45 g·kg^-1）， and high （NHQXW-H， 0.9 g·kg^-1） doses. Treatments were administered for 3 days after surgery. NHQXW effects on Tanre Fushi syndrome were assessed via fecal water content and small intestinal carbon propulsion rate. Protective effects of NHQXW against ICH with Tanre Fushi syndrome were evaluated by measuring hematoma volume， neurological deficits， and brain water content. BBB integrity was further assessed using Evans blue staining， hematoxylin-eosin （HE） staining， immunofluorescence， and Western blot for Claudin-5， plasmalemma vesicle-associated protein （PLVAP）， matrix metalloproteinase （MMP）-2， and MMP-9. The potential mechanism of NHQXW was investigated by detecting protein expression of protein kinase B （Akt）， extracellular signal-regulated kinase 1/2 （ERK1/2）， signal transducer and activator of transcription 3 （STAT3）， Yes-associated protein （YAP）， and their phosphorylated forms. ResultsCompared with the collagenase+feces group， NHQXW-M and NHQXW-H significantly reduced fecal water content （P<0.05， P<0.01） and intestinal propulsion rate （P<0.01）， alleviated neurological deficits （P<0.01）， decreased hematoma volume （P<0.01） and Evans blue extravasation （P<0.01）， increased Claudin-5 protein expression （P<0.05， P<0.01） and fluorescence intensity （P<0.01）， and decreased PLVAP protein expression （P<0.01） and fluorescence intensity （P<0.05， P<0.01）， as well as MMP-2 （P<0.05， P<0.01） and MMP-9 （P<0.01） expression. NHQXW-H downregulated p-Akt （P<0.05）， p-ERK1/2 （P<0.05）， p-STAT3 （P<0.01）， and p-YAP （P<0.05）， with the most significant effect observed on STAT3 phosphorylation. ConclusionNHQXW effectively alleviates neurological deficits and BBB injury in ICH mice with Tanre Fushi syndrome， primarily by inhibiting STAT3 activation.

Stroke is a neurological disease characterized by cerebral ischemia or hemorrhagic injury， leading to death and disability worldwide. At present， there is still a lack of neuroprotective drugs for the treatment of stroke. Niuhuang Qingxin pills are Chinese patent medicine recommended by guidelines and expert consensus for preventing and treating stroke. Studies have shown that Niuhuang Qingxin pills have sedative， anticonvulsant， antipyretic， and other pharmacological effects. Moreover， the main components， such as flavonoids， phenolic acids， and saponins， also exhibit strong pharmacological activities which can improve stroke-induced nerve damage. Studies have confirmed that representative ingredients such as baicalin and ginsenosides can interfere with multiple pathological events， including blood-brain barrier destruction， oxidative stress， inflammatory response， apoptosis， and autophagy， and the mechanisms of the essential ingredients are related to the action on important targets such as Kelch-like ECH-associated protein 1 （Keap1）， matrix metalloproteinase-9 （MMP-9）， and high-mobility group box 1 （HMGB1）， and involvement in the regulation of Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB）， nuclear factor E₂-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1）， and phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathways. This article summarized the research status of Niuhuang Qingxin pills and the experimental pharmacological progress of common ingredients in the prevention and treatment of stroke to provide clues for further research into Niuhuang Qingxin pills and the development of active ingredients of traditional Chinese medicines.

Objective To investigate the role of M2-type macrophages in interstitial fibrosis of kidney allograft.Methods The degree of interstitial fibrosis in renal biopsy tissues was assessed by Masson staining.By immunohistochemical double staining method and image analysis system,the levels of CD163 and SMA expression were detected in the renal biopsy tissues of 30 cases of CAI and 10 cases of normal kidney.The soluble CD163 was determined in urine by double antibody sandwich enzyme-linked immunosorbent assay.Results There were statistically significant differences in the expression of CD163 and SMA between kidney allograft and normal kidney tissue (P＜0.05).With the increase in renal fibrosis severity,the levels of serum Cr,BUN and the expression of CD163 and SMA were increased (P＜0.05).There was a positive correlation between the CD163 expression and the levels of serum Cr (r =0.937,P =0.000),and between the expression of CD63 and the level of sCD163 in urine.Conclusion The abnormal high expression of M2 macrophages in chronic renal allograft injury was associated with the degree of interstitial fibrosis and renal insufficiency in patients.