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1.
Front Immunol ; 14: 1087677, 2023.
Article in English | MEDLINE | ID: mdl-37168865

ABSTRACT

Inflammatory bowel disease (IBD) is a group of disorders that cause chronic inflammation in the intestines, with the primary types including ulcerative colitis and Crohn's disease. The link between autophagy, a catabolic mechanism in which cells clear protein aggregates and damaged organelles, and intestinal health has been widely studied. Experimental animal studies and human clinical studies have revealed that autophagy is pivotal for intestinal homeostasis maintenance, gut ecology regulation and other aspects. However, few articles have summarized and discussed the pathways by which autophagy improves or exacerbates IBD. Here, we review how autophagy alleviates IBD through the specific genes (e.g., ATG16L1, IRGM, NOD2 and LRRK2), crosstalk of multiple phenotypes with autophagy (e.g., Interaction of autophagy with endoplasmic reticulum stress, intestinal antimicrobial defense and apoptosis) and autophagy-associated signaling pathways. Moreover, we briefly discuss the role of autophagy in colorectal cancer and current status of autophagy-based drug research for IBD. It should be emphasized that autophagy has cell-specific and environment-specific effects on the gut. One of the problems of IBD research is to understand how autophagy plays a role in intestinal tract under specific environmental factors. A better understanding of the mechanism of autophagy in the occurrence and progression of IBD will provide references for the development of therapeutic drugs and disease management for IBD in the future.


Subject(s)
Colitis, Ulcerative , Crohn Disease , Inflammatory Bowel Diseases , Animals , Humans , Inflammatory Bowel Diseases/genetics , Crohn Disease/genetics , Inflammation/complications , Colitis, Ulcerative/complications , Autophagy/genetics
2.
Ann Transplant ; 23: 75-80, 2018 Jan 26.
Article in English | MEDLINE | ID: mdl-29371586

ABSTRACT

BACKGROUND This study aimed to evaluate the early and mid-term outcomes of drug-coated balloon (DCB) use in patients who underwent intervention for transplant renal artery stenosis (TRAS). MATERIAL AND METHODS We retrospectively reviewed the records of TRAS patients who received endovascular therapy with DCB in our institution from March 2016 to January 2017. Statistical analysis of pre-/postoperative levels of serum creatinine (Scr), systolic blood pressure (SBP), and renal artery peak systolic velocities (PSV) were performed. RESULTS Fourteen patients presenting with TRAS, which were mostly located at the anastomosis (n=9) and transplanted artery proximal portion (n=2), were treated with DCB. Three TRAS patients with in-stent restenosis (ISR) were also included in the series. The procedure technique success rate was 100%. The mean follow-up time was 8.6 months. The Scr level decreased from 481.8 µmol/L (208.5-746.2µmol/L) pre-operation to 154µmol/L (89.1-301.2 µmol/L, p<0.01) at 1 month post-intervention. The SBP varied from 161.4 mmHg (152-173 mmHg) to 144.8 mmHg (136-154 mmHg, p<0.01). Renal artery PSV decreased from 364.1 cm/s (217.6-511.9 cm/s) to 134.9 cm/s (79.8-184.2 cm/s, p<0.01). Eleven patients finished mid-term (>6 months) follow-up. The statistical results were not significant compared to those at 1 month, although they all slightly decreased. No re-intervention was performed. CONCLUSIONS The endovascular approach to TRAS with DCB was a safe and effective treatment for restore and maintain the artery flow and renal function in short-term follow-up.


Subject(s)
Endovascular Procedures/methods , Kidney Transplantation/adverse effects , Renal Artery Obstruction/therapy , Adult , Aged , Angioplasty, Balloon/methods , Creatinine/blood , Female , Humans , Male , Middle Aged , Renal Artery Obstruction/blood , Renal Artery Obstruction/etiology , Retrospective Studies , Treatment Outcome , Young Adult
3.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 34(6): 501-506, 2018 Jun 08.
Article in Chinese | MEDLINE | ID: mdl-31032584

ABSTRACT

OBJECTIVE: To study the effects of alcohol administration on benign prostate hyperplasia(BPH) and the reproductive toxicity during development of benign prostate hyperplasia. METHODS: Seventy adult male Kunming mice were randomly divided into seven groups:control (group CON), negative control (group NC, injected subcutaneously with soybean oil, 25 mg/(kg·d), intragastric administration of distilled water, 7.5 ml/(kg·d)), alcohol for 7 and 21 days (group AL7 and AL21, intragastric administration with wine of 50% alcohol, 7.5 ml/(kg·d)), testosterone propionate for 7 and 21 days (group TP7 and TP21, injected subcutaneously with testosterone propionate, 25 mg/(kg·d)), testosterone propionate+alcohol for 7 days (group TP+AL7, injected subcutaneously with testosterone propionate, 25 mg/(kg·d), and intragastric administration with wine of 50% alcohol, 7.5 ml/(kg·d)),10 mice in each groups. Twenty-four hours after the last administration, mice were sacrificed. The indexes of prostate and testis and the parameters of sperm were determined in mice. The levels of free radicals, antioxidation and histopathological changes in testis and prostate were determined. RESULTS: Compared with the control, TP7d group, AL7 and AL21d groups, the prostate coefficient of TP + AL7d group was increased significantly and the quantity and quality of sperm were decreased significantly (P<0.05), the content of MDA in prostate and testis was increased significantly, meanwhile the activities of SOD and GPx were decreased significantly (P< 0.05). Compared with TP21d group, the prostate coefficient of TP + AL7d group had no significant difference (P>0.05). CONCLUSIONS: The typical BPH state could be induced after 7-day treatment of testosterone propionate and alcohol. The testicular and sperm were damaged which enhanced the oxidative stress in reproductive system. The results indicated that alcohol could significantly promote the prostate hyperplasia induced by testosterone propionate in mice.


Subject(s)
Prostatic Hyperplasia , Animals , Male , Mice , Plant Extracts , Testosterone Propionate
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