Objective To investigate the effects of Yiqi Bushen Huoxue Jiangzhuo Formula on residual renal function(RRF),serum interleukin-6(IL-6),and C-reactive protein(CRP)levels in maintenance peritoneal dialysis(PD)patients with chronic renal failure(CRF).Methods Eighty CRF patients requiring maintenance PD treatment and meeting the traditional Chinese medicine diagnostic criteria of spleen-kidney qi deficiency and damp-phlegm stasis stagnation syndrome were enrolled from the Nephrology Department of Lu'an Traditional Chinese Medicine Hospital between July 2022 and July 2024.Patients were randomly divided into an observation group(n=40)and a control group(n=40)using a random number table.Both groups received standard maintenance PD and conventional western medical treatment,while the observation group additionally received Yiqi Bushen Huoxue Jiangzhuo Formula.The treatment duration for both groups lasted 6 months.Changes in RRF,serum levels of inflammatory markers(IL-6,CRP),and nutritional status indicators(hemoglobin[Hb],prealbumin[PA],albumin[ALB])were evaluated before and after treatment.Clinical efficacy was assessed.Results(1)After 6 months of treatment,the overall response rate in the observation group was 90.00％(36/40),while that in the control group was 67.50％(27/40).The intergroup comparison(by chi-square test)showed that the efficacy of the observation group was significantly superior to that of the control group,with a statistically significant difference(P＜0.05).(2)After treatment,the levels of blood urea nitrogen(BUN),serum creatinine(SCr),and RRF in both groups decreased compared to pre-treatment levels(P＜0.05).And the reduction in BUN and SCr of the observation group was significantly greater than that in the control group,while the reduction in RRF was significantly smaller than that in the control group,with all differences being statistically significant(P＜0.01).(3)After treatment,serum IL-6 and CRP levels in both groups decreased compared to pre-treatment levels(P＜0.05).And the reduction in serum IL-6 and CRP levels in the observation group was significantly greater than that in the control group,with statistically significant differences(P＜0.01).(4)After treatment,serum Hb,PA,and ALB levels in both groups increased compared to pre-treatment levels(P＜0.05).And the increase in serum Hb,PA,and ALB levels in the observation group was significantly greater than that in the control group,with statistically significant differences(P＜0.01).Conclusion Yiqi Bushen Huoxue Jiangzhuo Formula effectively preserves residual renal function,mitigates inflammation,and improves nutritional status in CRF maintenance PD patients with spleen-kidney qi deficiency and damp-phlegm stasis stagnation syndrome.

Objective To investigate the mechanism of sanguinarine(SA)for alleviating ulcerative colitis(UC)induced by dextran sodium sulfate(DSS)in mice.Methods Male C57BL/6 mouse models of 3.5%DSS-induced UC were randomized for treatment with 1,5 and 10 mg/kg SA by gavage,400 mg/kg sulfasalazine by gavage,or 10 mg/kg SA combined with intraperitoneal injection of 30 mg/kg ML385(a Nrf2 inhibitor).The changes in intestinal inflammation was assessed by monitoring weight changes,disease activity index(DAI)score,colon length measurement,and HE staining.After the treatments,the colon tissues were collected for detection of malondialdehyde(MDA)content using colorimetry,mRNA expressions of inflammatory factors using RT-qPCR,and the expressions of Nrf2,HO-1,Keap-1,p-p65,p65,occludin,and ZO-1 proteins were detected using Western blotting.Results SA treatment obviously alleviated weight loss,colon length shortening and DAI score increase and ameliorated structural destruction of the colon glands and colonic crypts in mice with DSS-induced UC.SA intervention significantly decreased the levels of TNF-α,IL-1β and IL-6 mRNA and lowered ROS and MDA levels in the colon tissue of UC mice.The mouse models receiving SA treatment showed significantly increased expressions of Nrf2,HO-1,occludin and ZO-1 and lowered expressions of Keap-1 and P-P65 in the colon tissue without significant changes of p65 expression,and these changes were SA dose-dependent.Treatment with ML385 obviously attenuated the effect of high-dose SA for improving UC in the mouse models.Conclusion SA can improve UC-like enteritis in mice possibly by activating the Nrf2 pathway and inhibiting the NF-κB pathway in the colon tissue.

Objective To investigate the effect of sanguinarine(SAN)on proliferation and ferroptosis of colorectal cancer cells.Methods SW620 and HCT-116 cells treated with different concentrations of SAN were examined for cell viability changes using CCK8 assay to determine the IC50 of SAN in the two cells.The inhibitory effects of SAN on proliferation,invasion and migration of the cells were evaluated using colony-forming assay and Transwell assays.ROS production in the treated cells was analyzed with flow cytometry,and lipid peroxide production was assessed by detecting malondialdehyde(MDA)level.Glutathione(GSH)levels in the cells were detected,and Western blotting was used to detect the expressions of ferroptosis-related proteins STUB1 and GPX4.Results SAN significantly inhibited the proliferation,invasion and migration of SW620 and HCT-116 cells.SAN treatment significantly promoted ROS production,increased intracellular MDA level,and lowered GSH level in the two cells(P<0.05).Western blotting showed that SAN significantly upregulated the expression of STUB1 and down-regulated the expression of its downstream protein GPX4(P<0.05).Conclusion SAN induces ferroptosis in colorectal cancer cells by regulating STUB1/GPX4,which may serve as a new therapeutic target for colorectal cancer.

Objective To investigate the mechanism of sanguinarine(SA)for alleviating ulcerative colitis(UC)induced by dextran sodium sulfate(DSS)in mice.Methods Male C57BL/6 mouse models of 3.5%DSS-induced UC were randomized for treatment with 1,5 and 10 mg/kg SA by gavage,400 mg/kg sulfasalazine by gavage,or 10 mg/kg SA combined with intraperitoneal injection of 30 mg/kg ML385(a Nrf2 inhibitor).The changes in intestinal inflammation was assessed by monitoring weight changes,disease activity index(DAI)score,colon length measurement,and HE staining.After the treatments,the colon tissues were collected for detection of malondialdehyde(MDA)content using colorimetry,mRNA expressions of inflammatory factors using RT-qPCR,and the expressions of Nrf2,HO-1,Keap-1,p-p65,p65,occludin,and ZO-1 proteins were detected using Western blotting.Results SA treatment obviously alleviated weight loss,colon length shortening and DAI score increase and ameliorated structural destruction of the colon glands and colonic crypts in mice with DSS-induced UC.SA intervention significantly decreased the levels of TNF-α,IL-1β and IL-6 mRNA and lowered ROS and MDA levels in the colon tissue of UC mice.The mouse models receiving SA treatment showed significantly increased expressions of Nrf2,HO-1,occludin and ZO-1 and lowered expressions of Keap-1 and P-P65 in the colon tissue without significant changes of p65 expression,and these changes were SA dose-dependent.Treatment with ML385 obviously attenuated the effect of high-dose SA for improving UC in the mouse models.Conclusion SA can improve UC-like enteritis in mice possibly by activating the Nrf2 pathway and inhibiting the NF-κB pathway in the colon tissue.

Objective To investigate the effect of sanguinarine(SAN)on proliferation and ferroptosis of colorectal cancer cells.Methods SW620 and HCT-116 cells treated with different concentrations of SAN were examined for cell viability changes using CCK8 assay to determine the IC50 of SAN in the two cells.The inhibitory effects of SAN on proliferation,invasion and migration of the cells were evaluated using colony-forming assay and Transwell assays.ROS production in the treated cells was analyzed with flow cytometry,and lipid peroxide production was assessed by detecting malondialdehyde(MDA)level.Glutathione(GSH)levels in the cells were detected,and Western blotting was used to detect the expressions of ferroptosis-related proteins STUB1 and GPX4.Results SAN significantly inhibited the proliferation,invasion and migration of SW620 and HCT-116 cells.SAN treatment significantly promoted ROS production,increased intracellular MDA level,and lowered GSH level in the two cells(P<0.05).Western blotting showed that SAN significantly upregulated the expression of STUB1 and down-regulated the expression of its downstream protein GPX4(P<0.05).Conclusion SAN induces ferroptosis in colorectal cancer cells by regulating STUB1/GPX4,which may serve as a new therapeutic target for colorectal cancer.