A total of 258 cases of elderly patients with herpes zoster were divided into treatment group (n =128) and control group (n =130).The treatment group received a once daily dose of narrowband ultraviolet irradiation plus oral acyclovir 0.8 g,5 times a day.However,the control group received a once daily dose of infrared therapy plus the same oral acyclovir.At Day 9,the effective rates of treatment and control groups were 91.7％ (117/128) vs.74.6％ (97/130) (P＜0.05).Also,in terms of pain relief time (2.56 ± 1.51) vs.(5.44 ±4.06) days,crusting time (4.51 ±0.48) vs.(6.11 ± 1.81) days and healing time (5.65 ±0.56) vs.(9.28 ±0.21) days,the treatment group was better than those of the control group (P ＜0.01).

AIM:To detect the activation of macrophage autophagy caused by lipopolysaccharide ( LPS) and the possible related signaling pathways .METHODS:The macrophage cell line RAW264.7 cultured in vitro was divided into 5 groups according to the culture environment , including normal culture group , starvation-activated sautophagy group , LPS group, LPS+PI3K inhibitor (hVps34) group and LPS+mTOR inhibitor (rapamycin) group.Fluorescent expression vector pcDNA3.1-GFP-LC3 constructed in previous work was transfected into the macrophages .The fluorescence microscopy was used to detect the formation of autophagosome .The mRNA expression of autophagy-associated genes Atg5, Atg7, LC3-II and Bnip3 in the macrophages was detected by qRT-PCR.The protein levels of LC3-II, p-Akt and p-mTOR were deter-mined by Western blotting , so as to evaluate the molecular pathways of autophagy in LPS-activated macrophages .RE-SULTS:The macrophages stably expressing GFP-LC3 were successfully established , which were used to observe the auto-phagy under fluorescence microscope .Compared with normal culture group , the autophagy in starvation group , LPS +hVps34 group and LPS+rapamycin group was significantly increased .The mRNA expression levels of Atg5, LC3-II and Bnip3 were significantly increased in starvation group , LPS+hVps34 group and LPS +rapamycin group , while in LPS group, those decreased slightly .The protein level of p-Akt in starvation group , LPS group and LPS+rapamycin group was significantly increased , while p-mTOR in starvation group , LPS+hVps34 group and LPS+rapamycin group significantly declined .LC3-II expression level in starvation group , LPS+hVps34 group and LPS+rapamycin group was higher than that in control group and LPS group .CONCLUSION: LPS regulates macrophage autophagy , and its possible pathway is the PI3K/Akt/mTOR pathway, but there are some other effective regulatory pathways .

OBJECTIVETo observe the impact of PDE5shRNA on cardiac remodeling and heart function following myocardial infarction in mice.

METHODSMyocardial infarction (MI) was induced in mice by left coronary artery ligation. Mice were randomly assigned to sham group (n = 6), PDE5shRNA group (n = 12), common adenovirus group (n = 15) and DMEM group (n = 8). Four weeks post-MI, the survival rate was evaluated. Cardiac function was examined by echocardiography. HE staining and Masson staining were used to evaluate the myocardial infarction size and fibrosis. The number of blood vessels was evaluated by immunohistochemistry, PDE5 protein expression in the left ventricular was detected using Western blot, level of cGMP or PKG activity in the left ventricle was evaluated with ELISA.

RESULTSFour weeks post-MI, all mice survived in the sham group, 3(37%) mice died in the DMEM group, 1 (8%) died in the PDE5shRNA group and 5 died in the common adenovirus group (33%). Infarct size was significantly reduced in PDE5shRNA group compared with the common adenovirus group and DMEM group [(25.4 ± 2.9)% vs. (42.0 ± 3.2)% and (43.4 ± 2.6) %, P < 0.05]. Cardiac function was significantly improved in PDE5shRNA group compared to common adenovirus group and DMEM group[LVFS: (21.1 ± 3.7)% vs. (14.2 ± 2.9)% and (14.22 ± 2.91)%, all P < 0.05; LVEF: (48.2 ± 7.1)% vs. (34.6 ± 6.2)% and (38.1 ± 2.8)%, all P < 0.05; LVESD: (3.87 ± 0.45) mm vs.(4.91 ± 0.62) mm and (4.63 ± 0.37) mm, all P < 0.05]. The blood vessel density was also higher in PDE5shRNA group compared with common adenovirus group (infarct area:14.3 ± 2.0 vs. 6.6 ± 1.2, P < 0.05; periinfarct area: 23.6 ± 2.1 vs. 13.7 ± 2.4, P < 0.05). Compared with common adenovirus group, level of PDE5 was significantly downregulated and level of cGMP or PKG was significantly upregulated in PDE5shRNA group (all P < 0.05).

CONCLUSIONSPresent study suggests PDE5shRNA improves cardiac function and attenuates cardiac remodeling through reducing infarction size and cardiac fibrosis and these beneficial effects are possibly mediated by activating cGMP/PKG signaling pathway.

Adenoviridae ; genetics ; Animals ; Cyclic Nucleotide Phosphodiesterases, Type 5 ; genetics ; Disease Models, Animal ; Heart Failure ; etiology ; therapy ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction ; complications ; RNA, Small Interfering ; genetics ; Ventricular Remodeling