1.The comparison between mild cases and severe cases of hand-foot-mouth disease
Guoshun MAO ; Ling LUO ; Xiaolin LIU ; Lichun WANG ; Lifeng LIU ; Zhifeng QIU ; Yang HAN ; Yong ZHAO ; Ying ZHU ; Jing XIE ; Qihan LI ; Taisheng LI
Chinese Journal of Infectious Diseases 2008;26(7):387-390
Objective To compare the simple cases of hand-foot-mouth disease(HFMD) with HFMD patients complicated with encephalitis and HFMD cases complicated with pulmonary edema (PE). To explore predictor factors of disease progression and unfavorable prognosis. Methods Forty-one EV71-infected children admitted to the Fuyang First People's Hospital in Anhui Province from March to May in 2008 were investigated in the research, who were classified as encephalitis-complicated cases ( encephalitis group, n = 15 ), PE-complicated cases ( PE group, n = 15 ) and simple cases (simple group, n= 11 ). Their clinical manifestation, laboratory findings, and immunophenotypes of peripheral blood lymphocyte were analyzed to find predictors associated with disease progression and unfavorable outcomes. Results The mortality rate in PE group was 66.7%, which was significantly higher than that in encephalitis group. Ninty-three point three percent cases in PE group and encephalitis group were younger than 3 years old, with statistic difference compared to simple group. Patients in PE group had higher total blood white cell (WBC) counts and higher absolute neutrophil counts and tended to have higher breathing rate, heart i'ate and glucose level than encephalitis group. The percentages of T cells and natural killer (NK) cells were significantly lower among patients complicated with encephalitis than simple HFMD patients.Conclusions PE is one predictor for poor prognosis. Factors correlated with unfavorable outcome include high WBC, high absolute neutrophil counts; elevated breathing rate, heart rate and glucose level. The immunophenotypes of peripheral blood lymphocytes can also predict the disease progression.
2.Shen Qi Wan attenuates renal interstitial fibrosis through upregulating AQP1.
Yiyou LIN ; Jiale WEI ; Yehui ZHANG ; Junhao HUANG ; Sichen WANG ; Qihan LUO ; Hongxia YU ; Liting JI ; Xiaojie ZHOU ; Changyu LI
Chinese Journal of Natural Medicines (English Ed.) 2023;21(5):359-370
Renal interstitial fibrosis (RIF) is the crucial pathway in chronic kidney disease (CKD) leading to the end-stage renal failure. However, the underlying mechanism of Shen Qi Wan (SQW) on RIF is not fully understood. In the current study, we investigated the role of Aquaporin 1 (AQP1) in SQW on tubular epithelial-to-mesenchymal transition (EMT). A RIF mouse model induced by adenine and a TGF-β1-stimulated HK-2 cell model were etablished to explore the involvement of AQP 1 in the protective effect of SQW on EMT in vitro and in vivo. Subsequently, the molecular mechanism of SQW on EMT was explored in HK-2 cells with AQP1 knockdown. The results indicated that SQW alleviated kidney injury and renal collagen deposition in the kidneys of mice induced by adenine, increased the protein expression of E-cadherin and AQP1 expression, and decreased the expression of vimentin and α-smooth muscle actin (α-SMA). Similarly, treatmement with SQW-containing serum significantly halted EMT process in TGF-β1 stimulated HK-2 cells. The expression of snail and slug was significantly upregulated in HK-2 cells after knockdown of AQP1. AQP1 knockdown also increased the mRNA expression of vimentin and α-SMA, and decreased the expression of E-cadherin. The protein expression of vimentin increased, while the expression of E-cadherin and CK-18 significantly decreased after AQP1 knockdown in HK-2 cells. These results revealed that AQP1 knockdown promoted EMT. Furthermore, AQP1 knockdown abolished the protective effect of SQW-containing serum on EMT in HK-2 cells. In sum, SQW attentuates EMT process in RIF through upregulation of the expression of AQP1.
Drugs, Chinese Herbal/pharmacology*
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Humans
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Animals
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Mice
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Male
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Cell Line
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Rats
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Kidney/physiology*
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Fibrosis/drug therapy*
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Renal Insufficiency, Chronic/drug therapy*
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Adenine
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Epithelial-Mesenchymal Transition
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Aquaporin 1/metabolism*