AIM:To explore the therapeutic effect and possible molecular mechanisms of prednisone combined with icariin(ICA)on hormone resistant nephrotic syndrome(SRNS).METHODS:In the in vi-vo experiment,rats were divided into control group,SRNS group,prednisone group,and P+I group.Each group was given corresponding drugs for 6 weeks.Detection of 24-hour urinary protein in rats using CBB;The blood biochemistry analyzer de-tects rat albumin,total cholesterol,triglycerides,creatinine,and urea nitrogen;HE and Masson were used to detect morphological changes in rat kidney tissue;Immunohistochemical detection of GR-α,GR-β,NLRP3,caspase-1,GSDMD,IL-1β.In the in vi-tro experiment,HK-2 cell injury model with doxoru-bicin,divided into control group,SRNS group,pred-nisone group,P+l group.GR-α,GR-β,NLRP3,cas-pase-1,GSDMD were detected by Rt-PCR and West-ern blot.RESULTS:In the in vivo experiment,com-pared with the control group,the SRNS group showed weight loss,increased 24-hour urine pro-tein,decreased albumin,increased total cholester-ol,triglycerides,creatinine,and urea nitrogen,renal tubular atrophy,increased renal interstitial area,sig-nificant infiltration of inflammatory cells,fibrous tis-sue proliferation,and GR-β,NLRP3,caspase-1,GSD-MD,IL-1 β in renal tissue decreased(P＜0.01);Com-pared with the SRNS group,the combined group showed weight gain,decreased 24-hour urine pro-tein,increased albumin,decreased total cholester-ol,triglycerides,creatinine,and urea nitrogen,re-duced renal tubular atrophy,reduced interstitial in-flammatory cell infiltration,reduced fibrosis,and and GR-α,NLRP3,caspase-1,GSDMD in renal tissue decreased increased(P＜0.01).In vitro experiments,compared with the control group,the model group showed GR-β,NLRP3,caspase-1,and GSDMD in-creased(P＜0.01),GR-α decreased(P＜0.01);Com-pared with the SRNS group,GR-β,NLRP3,caspase-1,and GSDMD decreased(P＜0.01),GR-α increased in the P+I group.CONCLUSION:The combination of prednisone and ICA has a protective effect on the kidneys of SRNS rats and can improve the therapeu-tic effect.The mechanism may be related to the NL-RP3/Caspase-1/GSDMD pathway.

Objective To investigate the efficacy of cognitive-behavioral therapy for insomnia (CBT-i) or combination with tapered hypnotic agents. Methods Seventy-five patients were randomized into either CBT-i group (n=37) or combination group (n=38). The duration of treatment lasted for 8 weeks. The efficacy was evaluated by Pittsburgh sleep quality index (PSQI),Beck depression index (BDI),Beck anxiety inventory(BAI) and sleep diary variables at baseline, middle and end of treatment. Results (1)Compared with the results at baseline, the total scores of PSQI,BDI and BAI in both groups significantly decreased at the end of treatment: CBT-i group, PSQI (4.7±2.5) vs. (12.9±3.5); BDI (3.2±4.4) vs. (9.7±6.4); BAI (4.2±5.6) vs. (10.7±8.1); and combination group, PSQI (5.8±2.8) vs. (13.9±3.1); BDI (4.5±4.8) vs. (13.8±8.7); BAI (4.4±4.0) vs. (14.1±6.3) (all P<0.01). (2) Compared with the results at baseline, subjective sleep quality (SQ), sleep onset latency (SOL), sleep efficiency (SE), sleep disturbance (SD) and used sleep medication (USM) in PSQI in combination group significantly decreased at week 4 and 8 (all P<0.05). The total sleep time (TST) and daytime dysfunction (DF) in PSQI significantly decreased at week 8 (both P<0.05). (3) Compared with combination group, improvement of SOL and SE in CBT-i group was superior (both P=0.01). Conclusions CBT-i for chronic insomnia is effective in both CBT-i alone and combination with tapered hypnotic agents. CBT-i group is superior in improving SOL and SE. Combination regimen in our study can significantly reduce the doses of medication.

Objectives To evaluate the effectiveness of cognitive behavior therapy for insomnia (CBT-i) in chronic insomnia patients in terms of the improvements of psychological and sleep diary parameters. Methods Patients who met the diagnostic criteria of chronic insomnia, were divided into primary group or comorbid group. Both groups received standard CBT-i interventions. Psychological scales and sleep diaries were used to evaluate participants' severity of insomnia and psychological conditions related to insomnia at four time points:before intervention (baseline), immediate after intervention, 4 weeks and 16 weeks after intervention. Results Both groups achieved significant improvements after intervention on psychological measurements and sleep diary parameters. Such improvements were maintained at 4-week and 16-week follow-ups. The sleep diary data indicated that by the end of the intervention, there were significant differences on sleep onset latency(51.72 min to 10.53 min in primary group, P<0.01;59.26 min to 15.67min in comorbid group, P<0.01)and sleep efficiency (71％to 95％in primary group, P<0.01;68％to 90％in comorbid group, P<0.01). There were differences on sleep onset latency (10.00 min vs. 13.93 min,P<0.05), total sleep time (355.71 min vs. 327.85 min, P<0.05) and sleep efficiency (95％vs. 91％, P<0.01) in primary group and comorbid group respectively. No differences were found on wake after sleep onset in the two groups. Conclusions Chronic insomnia patients with or without comorbidities both have improvements after CBT-i. Sleep diary parameters rather than psychological measurements are different in two groups. Thus, CBT-i is an effective non-pharmaceutical therapy inpatients with chronic insomnia.

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