To investigate whether the coexistence of hypertension and ovariectomy will increase cardiac Fas receptor and mitochondrial-dependent apoptotic pathways, histopathological analysis, the TUNEL assay and Western blotting were performed on the excised hearts from three groups of female spontaneously hypertensive rats (SHR), which were divided into a sham-operated group (SHR-Sham), bilaterally ovariectomized group (SHR-OVX) and normotensive Wistar Kyoto rats (WKY). Compared with the WKY group, the SHR-Sham group exhibited decreased protein levels of ERα, ERβ, p-Akt/Akt, Bcl-2, Bcl-xL and p-Bad and decreased further in the SHR-OVX group, as well as protein levels of t-Bid, Bak, Bad, Bax, cytochrome c, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptosis) increased in the SHR-Sham group and increased further in the SHR-OVX group. Compared with the WKY group, protein levels of Fas ligand, TNF-α, Fas death receptors, TNFR1, FADD and activated caspase-8 (Fas receptor-dependent apoptosis) increased in the SHR-Sham group, but did not increase in the SHR-OVX group, except Fas ligand and TNF-α. The coexistence of hypertension and ovariectomy attenuated the estrogen receptor survival pathway and appeared to additively increase the cardiac mitochondria-dependent, but not the Fas receptor-dependent apoptosis pathway, which might provide one possible mechanism for the development of cardiac abnormalities in hypertensive postmenopausal women.

Patients with diabetes mellitus (DM) are at high risk of developing peripheral arterial obstructive disease (PAOD) in lower extremities. Previous studies show low level LASER therapy (LLLT) can increase angiogenesis in vivo and in vitro. Here we performed hindlimb ischemia as PAOD model on diabetic mice to test the effects of LLLT. Twenty C57Bl/6 mice were randomly divided into four groups. Control group mice received femoral artery ligation/excision only. DM group mice were injected with Streptozocin (STZ) to induce diabetes followed by femoral artery ligation/excision. LLLT group mice received femoral artery ligation/excision and the lower limbs received LASER treatment for five days (660nm, 10 min, 1.91 J/cm2) started from second day postoperatively. DM+LLLT group mice were received femoral artery ligation/excision and LASER treatment after diabetes induced. Three days after LASER treatment finished, limb blood flow was measured by Laser Doppler perfusion imaging. Capillary density was assessed by immunofluorescence staining. CD31, VEGF, HIF-1?, phospho-ERK, iNOS and eNOS protein level was examined by Western blot. Blood perfusion, capillary density, CD31, and VEGF protein levels were significantly higher in those groups received LLLT compared to control and DM group. Low level LASER significantly increased ERK phosphorylation and HIF-1? expression. In addition, phospho-eNOS was increased but iNOS protein level was decreased in mice received LASER treatment. In summary, the ability of low level LASER to induce therapeutic angiogenesis in diabetic mice suggested this approach deserves investigation as a novel approach to treat PAOD patients.