OBJECTIVEThe pathogenesis of minimal change nephrotic syndrome (MCNS) remains unclear. This study aimed to investigate the expression of interleukin-6 (IL-6) in rats with doxorubicin-induced nephropathy and its possible roles in the pathogenesis of MCNS.

METHODSEighty-three male Wistar rats were randomly assigned into a control group (n=32) and a nephropathy group (n=51). Nephropathy was induced by a single tail vein injection of doxorubicin (5 mg/kg). The control group was injected with normal saline. Twenty-four-hour urinary protein excretion was measured 7, 14, 28 and 42 days after doxorubicin injection. IL-6 expression in urine and renal tissues was determined using ELISA 7, 14, 28 and 42 days after doxorubicin injection.

RESULTSThe urinary protein excretion increased significantly in the nephropathy group 7, 14, 28 and 42 days after doxorubicin injection compared with that in the control group (P<0.01). IL-6 expression in urine and renal tissues increased significantly 7, 14, 28 and 42 days after doxorubicin injection compared with that in the control group (P<0.01). IL-6 expression in urine and renal tissues was positively correlated with 24-hour urinary protein excretion in the nephropathy group (r=0.794, P<0.01; r= 0.870, P<0.01). IL-6 expression in urine was positively correlated with that in renal tissues (r=0.739, P<0.01).

CONCLUSIONSIL-6 expression in the urine and renal tissues is increased in MCNS rats. IL-6 might play an important role in the pathogenesis of MCNS.

Animals ; Antibiotics, Antineoplastic ; toxicity ; Disease Models, Animal ; Doxorubicin ; toxicity ; Interleukin-6 ; analysis ; Kidney ; chemistry ; Male ; Nephrosis, Lipoid ; chemically induced ; immunology ; Rats ; Rats, Wistar

Humans ; Diabetes Mellitus, Type 2/genetics* ; Gene-Environment Interaction ; Polymorphism, Single Nucleotide

BACKGROUND: Penehyclidine is a newly developed anticholinergic agent. We aimed to investigate the role of penehyclidine in acute organophosphorus pesticide poisoning (OP) patients. METHODS: We searched the Pubmed, Cochrane library, EMBASE, Chinese National Knowledge Infrastructure (CNKI), Chinese Biomedical literature (CBM) and Wanfang databases. Randomized controlled trials (RCTs) recruiting acute OP patients were identified for meta-analysis. Main outcomesincluded cure rate, mortality rate, time to atropinization, time to 60% normal acetylcholinesterase (AchE) level, rate of intermediate syndrome (IMS) and rate of adverse drug reactions (ADR). RESULTS: Sixteen RCTs involving 1,334 patients were identified. Compared with the atropine-or penehyclidine-alone groups, atropine combined with penehyclidine significantly increased the cure rate (penehyclidine+atropine vs. atropine, 0.97 vs. 0.86, RR 1.13, 95% CI [1.07–1.19]; penehyclidine+atropine vs. penehyclidine, 0.93 vs. 0.80, RR 1.08, 95% CI [1.01–1.15]) and reduced the mortality rate (penehyclidine+atropine vs. atropine, 0.015 vs. 0.11, RR 0.17, 95% CI [0.06–0.49]; penehyclidine+atropine vs. penehyclidine, 0.13 vs. 0.08, RR 0.23, 95% CI [0.04–1.28]). Atropine combined with penehyclidine in OP patients also helped reduce the time to atropinization and AchE recovery, the rate of IMS and the rate of ADR. Compared with a single dose of atropine, a single dose of penehyclidine also significantly elevated the cure rate, reduced times to atropinization, AchE recovery, and rate of IMS. CONCLUSION Atropine combined with penehyclidine benefits OP patients by enhancing the cure rate, mortality rate, time to atropinization, AchE recovery, IMS rate, total ADR and duration of hospitalization. Penehyclidine combined with atropine is likely a better initial therapy for OP patients than atropine alone.