ABSTRACT
Transglutaminase 2 (TGM2) is a ubiquitous multifunctional protein, which is related to the adhesion of different cells and tumor formation. Previous studies found that TGM2 is involved in the interaction between host cells and viruses, but the effect of TGM2 on the proliferation of influenza virus in cells has not been reported. To explore the effect of TGM2 during H1N1 subtype influenza virus infection, a stable MDCK cell line with TGM2 overexpression and a knockout cell line were constructed. The mRNA and protein expression levels of NP and NS1 as well as the virus titer were measured at 48 hours after pot-infection with H1N1 subtype influenza virus. The results showed that overexpression of TGM2 effectively inhibited the expression of NP and NS1 genes of H1N1 subtype influenza virus, while knockout of TGM2 up-regulated the expression of the NP and NS1 genes, and the expression of the NP at protein level was consistent with that at mRNA level. Virus proliferation curve showed that the titer of H1N1 subtype influenza virus decreased significantly upon TGM2 overexpression. On the contrary, the virus titer in TGM2 knockout cells reached the peak at 48 h, which further proved that TGM2 was involved in the inhibition of H1N1 subtype influenza virus proliferation in MDCK cells. By analyzing the expression of genes downstream of influenza virus response signaling pathway, we found that TGM2 may inhibit the proliferation of H1N1 subtype influenza virus by promoting the activation of JAK-STAT molecular pathway and inhibiting RIG-1 signaling pathway. The above findings are of great significance for revealing the mechanism underlying the interactions between host cells and virus and establishing a genetically engineering cell line for high-yield influenza vaccine production of influenza virus.
Subject(s)
Animals , Dogs , Humans , Cell Proliferation , Influenza A Virus, H1N1 Subtype/genetics , Influenza, Human , Madin Darby Canine Kidney Cells , Protein Glutamine gamma Glutamyltransferase 2ABSTRACT
Objective To investigate the effects of losartan on aortic elasticity and remodeling in spontaneously hypertensive rats (spontaneously hypertensive rats SHR). Methods WKY (Wistar - Kyoto ) rats with normal blood pressure and 16 weeks spontaneously hypertensive rats were randomly divided into WKY control group, SHR control group, high dose losartan group (SHR + HL), low doses losartan group (SHR + LL). Each group has six animals which were given normal diet for 24 weeks. Losartan which was dissolved in 10 ml physiological saline was filling in stomach, other groups were filling with physiological saline. Tail arterial blood pressure, kidney tissues calcium concentration, renal small artery hydroxyproline content was measured and small arteries wall thickness of Glomerularwas detected, and the ratio of thickness and inner diameter (MT/LR) in kidney pathological were observed. Results The calcium concentration of SHR group in kidney tissues was [(18.42±2.34)μmol/g], kidney small artery hydroxyproline content was [(8.26±2.02)mg/g], which were greater than WKY group [(11.83±1.98)μmol/g,(5.16±0.98)mg/g] (t＝3.116,3.258,P＜0.05), but the two treatment groups were less than SHR group (t＝2.946,P＜0.05), the difference was significant. Small arteries wall thickness of Glomerular was [(5.25±1.13)μm], the ratio of thickness and inner diameter (MT/LR) was [(9.57±1.78)%], which were greater than WKY group[(4.03±0.16)μm ,(7.12±1.35)%](t＝2.836,3.425,P＜0.05), but the wall thickness of two treatment groups were [(7.64±1.29)%,(7.85±1.32)%], the two treatment groups were less than SHR group (t＝3.512,3.648,P＜0.05). Conclusions Losartanmay inhibit intracellular calcium overload, reduce fibrosis degree and improve renal arteriole resistance and reverse the renal arteriole reconstruction of SHR rats.
ABSTRACT
It has been well-documented that ICAM-1 implicates in pathophysiology of ischemic-reperfusion injury of the kidney.Renal injury after ischemia appears to be a consequence of tissue hypoxia not only from interrupted blood supply but also from the process of reperfusion which leads to an active inflammatory process.Infiltrating leukocytes are potential source of reactive oxygen species.Proteolytic enzymes and cytokines,which during reperfusion may play a detrimental role.It has been suggested that ICAM-1 plays a key role during leukocyte adhesion and recruitment to inflamed tissue.The goal of the review is to explore the effect and significance of ICAM-1 as well as its mechanism in renal ischemia-reperfunsion.
ABSTRACT
OBJECTIVE: To observe the clinical efficacy of Shenyan kangfu tablet combined with benazepril in the treatment of chronic nephritis. METHODS: 160 chronic nephritis patients with healthy renal function were randomly divided into benazepril (ACEI) group and Shenyan kangfu tablet combined with benazepril group (combination group). 24 hour urinary protein, blood pressure and creatinine of 2 groups were determined before and after treatment. RESULTS: After 4 months of treatment, the total effective rates were 87.5% for combination group and 56.25% for ACEI group (P0.05). CONCLUSION: Shenyan kangfu tablet combined with benazepril can reduce proteinuria in patients with chronic nephritis,non-toxic side effect in short-term.