Objective To explore the influences of hydrogen sulfide （H2S） on acute necrotizing pancreatitis （ANP）. Methods Forty-three SD male rats were grouped by random number table， and divided into five groups：the sham group （n=4）， ANP group 〔n=21， which was divided into 3 subgroups：3， 6， and 12 hours group （n=7）〕， NaCl＋ANP group （n=4）， NaHS＋ANP group （n=7）， and PAG＋ANP group （n=7）. Models of ANP were formed byretrograde cholangiopancreatography injection of 5% sodium taurocholate. The NaCl＋ANP group， NaHS＋ANP group， and PAG＋ANP group rats were given pretreatment of saline， NaHS， or PAG at 1 hour before modelingrespectively. The levels of serum amylase （AMY）， aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， blood urea nitrogen （BUN）， and creatinine （Cr） were detected， and the pathological histological changes of pancreatic tissues were observed. Results The levels of serum AMY， AST， ALT， BUN， and Cr were increased in ANP group. The levels of serum AMY， AST， ALT， BUN， and Cr in the NaHS＋ANP group were higher than those of NaCl＋ANP group （P＜0.05）， and the pathological damage of the pancreatic tissues was more serious in the NaHS＋ANP group. The levels of serum AMY， AST， ALT， BUN， and Cr in the PAG＋ANP group were lower than those of NaCl＋ANPgroup （P＜0.05）， and the pathological damage of pancreatic tissues in the PAG＋ANP group was not so serious as in the NaCl＋ANP group. Conclusions The impairment of liver， kidney， and pancreas function in ANP rats may be related to elevated H2S concentration. Prophylactic administration the PAG of H2S antagonist can improve the function of the liver， kidney， and pancreas， and have the effects of organ protection.
ObjectiveTo investigate the potential role and mechanism of hydrogen sulfide (H2S) in regulating arterial baroreflex (ABR) in septic rats. MethodsThe rat model of cecal ligation and puncture (CLP) induced sepsis was established. Fortyseven male SpargueDawley rats were randomly divided into 9 groups: ① Sham operation (SO)+0.9% NaCl (NS) intravenous injection (i.v.) group; ② SO+NaHS i.v. group; ③ CLP+NaHS i.v. group; ④ SO+artificial cerebrospinal fluid (aCSF) bilater nucleus tractus solitarii (NTS) microinjection group; ⑤ SO+NaHS bilater NTS microinjection group; ⑥ SO+vehicle (DMSO)+NaHS group; ⑦ SO+Gli+NaHS group; ⑧ CLP+vehicle (DMSO) group; ⑨ CLP+Gli group. The ABR function was measured before administration and 5 min and 30 min after administration. Results① The ABR value of rats at different time in the same group: Compared with the ABR value before administration in the SO+NaHS i.v. group, CLP+NaHS i.v. group, SO+NaHS bilater NTS microinjection group, and SO+vehicle+NaHS group, the ABR values of rats significantly decreased at 5 min and 30 min after administration (Plt;0.05, Plt;0.01), which significantly increased in the CLP+Gli group at 5 min and 30 min after administration (Plt;0.05). ② The ABR value of rats at the same time in the different groups: Before administration, the ABR value of rat in the CLP+NaHS i.v. group was significantly lower than that in the SO+NS i.v. group or SO+NaHS i.v.group (Plt;0.05). At 5 min and 30 min after adminis tration, the ABR value of rat in the CLP+NaHS i.v. group was significantly lower than that in the SO+NS i.v. group or SO+NaHS i.v. group (Plt;0.05), which in the SO+NaHS i.v. group or SO+NaHS bilater NTS microinjection group was significantly lower than that in the SO+NS i.v. group or SO+aCSF bilater NTS microinjection group, respectively (Plt;0.05, Plt;0.01), in the SO+Gli+NaHS group or CLP+Gli group was significantly higher than that in the SO+vehicle+NaHS group or CLP+vehicle group, respectively (Plt;0.05). ConclusionsH2S plays an adverse role in septic ABR function, and opening KATP channel located at the pathway of ABR, may be the mechanism involved in the downregulation of ABR function in septic rat. Notably, the NTS may be also responsible for reduction of ABR value.
ObjectiveTo investigate the distribution and content of endogenous salusin-βin septic rats. MethodsThirty-six SPF male SD rats were randomly divided into sham operation group (n=9) and septic model group (n=27).Only the cecum was turn in the sham operation group and the septic model was made by the cecal ligation and puncture (CLP) in the septic model group.The rats were sacrificed at 6 h, 12 h, and 24 h after modeling in the septic model group.The contents of salusin-βin the tissues of spleen, stomach, small intestine, hypothalamus, and serum specimens were detected by enzyme-linked immunosorbent assay. Results①The salusin-βendogenously generated in the rat tissues including the spleen, stomach, small intestine, hypothalamus, and serum.The content of salusin-βin the spleen tissue was higher than that in the other tissues (P < 0.05).②The contents of salusin-βin the spleen, stomach, small intestine tissues together with the serum increased significantly at 6 h after CLP as compared with the sham operation group (P < 0.05).The contents of salusin-βin the spleen tissue and serum were peaked at 12 h, in the small intestine tissue reached the summit at 24 h.While, the content of salusin-βhad no significant fluctuation in the stomach tissue.The content of salusin-βbegan to increase at 6 h in the hypothalamus tissue, and significantly increased at 12 h after CLP (P < 0.05). ConclusionThe time-dependent change of salusin-βin sepsis rats suggests that salusin-βmight be involved with the pathogenesis of sepsis.
ObjectiveTo summarize the anti-inflammatory effects of irisin in inflammatory diseases.MethodThe relevant literatures at home and abroad in recent years were systematically searched and read to review the anti-inflammatory effects of irisin in the inflammatory diseases.ResultsThe irisin was widely distributed in the body and played a physiological role in inducing the browning of white adipocytes, improving energy metabolism and glucose utilization. A grow body of evidences demonstrated that the irisin exerted the anti-inflammatory effects by inhibiting increased pro-inflammatory cytokines and tumor necrosis factor-α, antagonizing apoptosis and activation of nuclear factor-κB, and improving tissue damage in many inflammatory diseases, such as acute lung injury, inflammatory bowel disease, septic cardiomyopathy, acute pancreatitis, nonalcoholic fatty liver disease, and malignant tumors.ConclusionsIrisin plays an important anti-inflammatory role in pathogenesis of inflammatory diseases. Irisin is considered as a promising candidate biomarker for diagnosis and prognosis of inflammatory diseases, and a novel target for treatment of inflammatory diseases.