Objective
To determine the expression of silent information regulator 1 (SIRT1), superoxide dismutase (SOD), malondialdehyde (MDA) and the GSH, the aim of this study is to investigate the effects of the berberine to the expression of the SIRT1 protein and the protective effects to the liver function as related to cholestatic liver injury in rats.
Methods
The rats were divided randomly into three groupls (n=15): the Sham group receiving laparotomy without bile duct ligation (BDL), the BDL group and the BDL+ BBR group with the berberine (BBR) given following BDL. The expression of the SIRT1 proteins were analyzed by western blotting and the PCR was performed to determine the mRNA expression of SIRT1 in all groups. The kits of SOD, MDA and GSH were used to detect the values in liver tissue and the apoptosis of the liver cells was examined by TdT-mediated dUTP nick end labeling (TUNEL) staining.
Results
The levels of the mRNA and proteins of the SIRT1, SOD and GSH in BDL group [(0.13±0.01), (0.16±0.02), (243.49±27.52) U/mg, (27.42±4.39) mg/g] were significantly lower than in BDL+ BBR group [(0.41±0.03), (0.27±0.01), (331.25±26.93) U/mg, (35.38±4.65) mg/g; P<0.01] and in Sham group [(0.68±0.09), (0.32±0.04), (294.47±25.82) U/mg, (36.82±3.47) mg/g; P<0.01], while the alanine aminotransferase (ALT), malondialdehyde (MDA) and the apoptosis rate [(235.63±13.34) IU/L, (0.92±0.27) nmol/mg, (13.00±0.04)%] were significantly higher in BDL+ BBR group [(148.27±13.98) IU/L, (0.61±0.09) nmol/mg, (6.21±0.02)%; P<0.05] and in Sham group [(39.13±4.39) IU/L, (0.72±0.07) nmol/mg, (0.06±0.00)%, P<0.01].
Conclusion
The present study demonstrates that the BBR could protect the liver from the peroxide damage by increasing the expression of the SIRT1 which could promote the expression of the gene of SOD.
Key words:
Berberine; Cholestasis; Silent Information Regulator 1; Superoxide Dismutase; Malondialdehyde
Objective
To determinethe expression of silent information regulator 1(SIRT1), superoxide dismutase(SOD), malondialdehyde(MDA)and the glutathione(GSH), the aim of this study is to investigate the effects of the berberine to the expression of the SIRT1 protein and the protective effects to the renal function as related to cholestatic kidney injury in rats.
Methods
The animals were divided randomly into three groupls(n= 15).A rat model of cholestasis was established by bile duct ligation(BDL, B group)and compared with a Sham group receiving laparotomy without BDL(Sham, A group), and with the the BBR given respectively following BDL(BDL+ BBR, C group). All rats were sacrificed on the 7th day after BDL and the blood and kidney tissue samples were obtained.The expression of the SIRT1 proteins were analyzed by western blotting and the reverse transcriptase-polymerase chain reaction(RT-PCR)was performed to determine the mRNA expression of SIRT1 in all groups.The kits of SOD, MDA and GSH were used to detect the values in renal tissue and the apoptosis of the kidney cells was examined by Td T-mediated dUTP nick end labeling(TUNEL)staining.
Results
After the bile duct ligation, the model of cholestasis was established. Comparedto A group, the levels of the mRNA and proteins of the SIRT1,SOD and GSH were lower but the alanine transaminase(ALT), MDA and the apoptosis rate were higher in group B(P< 0.05). Compared C groups to B group, the levels of the mRNA and proteins of the SIRT1, SOD and GSH were higher but the MDA and the apoptosis rate were lower(P<0.05).The values of BUN,Cr,SOD,GSH,SIRT1 mRNA and protein and the rate of the A,Band C groups are:A group(3.14±0.53)mmol/L,(31.32±11.08)μmol/L, (19.45±2.41)nu/mg,(2.31±0.14)nmol/g,1.00±0.00, 0.27±0.01,(0.28±0.13)%; B group(8.37 ±1.57)mmol/L,(102.43±9.32)μmol/L,(5.96±1.43) nu/mg,(1.39±0.25) nmol/g, 0.51±0.05, 0.17±0.01,(19.36±2.56)%; C group(6.04±1.52) mmol/L,(78.58±13.63)μmol/L,(13.52±1.47) nu/mg,(1.97±0.19)nmol/g,0.79±0.04,0.22±0.01,(11.47±3.61)% the group A,B and C.
Conclusion
The present study demonstrates that the BBR could protect the kidney from the peroxide damage by increasing the expression of the SIRT1 which could promote the expression of the gene of SOD. And so the BBR plays a benefical role to resist peroxide damage and apoptosis in cholestatickidney injury.
Key words:
Berberine; Cholestasis; Silent information regulator 1; Superoxide dismutase
Bladder cancer is characterized by high rates of recurrence and multifocality. Immunogenic cell death (ICD) of cancer cells has emerged as a promising strategy to improve the immunogenicity of tumor cells for enhanced cancer immunotherapy. Although photosensitizer-based photodynamic therapy (PDT) has been validated as capable of inducing ICD in cancer cells, the photosensitizers with a sufficient ICD induction ability are still rare, and there have been few reports on the development of advanced photosensitizers to strongly evoke the ICD of bladder cancer cells for eliciting potent antitumor immune responses and eradicating bladder carcinoma in situ. In this work, we have synthesized a new kind of endoplasmic reticulum (ER)-targeting aggregation-induced emission (AIE) photosensitizer (named DPASCP-Tos), which could effectively anchor to the cellular ER and trigger focused reactive oxygen species (ROS) production within the ER, thereby boosting ICD in bladder cancer cells. Furthermore, we have demonstrated that bladder cancer cells killed by ER-targeted PDT could serve as a therapeutic cancer vaccine to elicit a strong antitumor immunity. Prophylactic vaccination of the bladder cancer cells killed by DPASCP-Tos under light irradiation promoted the maturation of dendritic cells (DCs) and the expansion of tumor antigen-specific CD8
Cancer is still a global public health problem. Although remarkable success has been achieved in cancer diagnosis and treatment, the high recurrence and mortality rates remain severely threatening to human lives and health. In recent years, peptide nanomedicines with precise selectivity and high biocompatibility have attracted intense attention in biomedical applications. In particular, there has been a significant increase in the exploration of peptides and their derivatives for malignant tumor therapy and diagnosis. Herein, we review the applications of peptides and their derivatives in the diagnosis and treatment of bladder cancer, providing new insights for the design and development of novel peptide nanomedicines for the treatment of bladder cancer in the future.
Objective To explore the protective mechanism and effect of the resveratrol (Res) for liver injury of obstructive jaundice.Methods The rats were divided randomly into three groups:the sham group receiving laparotomy without bile duct ligation (BDL),the BDL group and the BDL + Res group with the Res given following BDL.The expression of the silent information regulator 1 (SIRT1) and nuclear factor-κBp56 (NF-κB) proteins were analyzed by western blotting but immunocytochemical assay was performed to examine peroxisome proliferator activated receptor-alpha (PPARα) protein.Real-time polymerase chain reaction (PCR) was performed to determine the mRNA expression of SIRT1 and PPARα.Cell apoptosis was examined by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining.Results After the BDL,the cholestasis model was established.Compared B group to A group,the alanine transaminase (ALT) was higher and the mRNA and proteins expression of the SIRT1 and the PPARα was lower,but the NF-κB protein and the rate of cell apoptosis was higher (P ＜ 0.05).Compared B group to C group,the ALT was higher and the mRNA and proteins expression of the SIRT1 and the PPARα was lower,but the NF-κB protein and the rate of cell apoptosis was significantly higher (P ＜ 0.05).Conclusion This study demonstrates that the Res could alleviate liver damage and that the Res plays a beneficial role to resist inflammation and apoptosis by activating the SIRT1 which probably inhibits the expression of NF-κB protein in cholestatic liver injury.The Res also shows antioxidant effect by promoting the expression of PPARα.
Key words:
Resveratrol; Cholestasis; Silent information regulator 1 ; Peroxisome proliferator activated receptor-alpha; Nuclear factor-κBp56
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)