RESUMO
Abnormally high follicle-stimulating hormone (FSH) has been reported to associate with cardiovascular diseases in prostate cancer patients with specific androgen deprivation therapy and in menopausal women. All of the cardiovascular diseases were involved in atherosclerosis. However, the pathogenic mechanism of FSH-associated atherosclerosis remains uncertain. Apolipoprotein E-deficient mice were chosen to develop atherosclerosis, of which the plaques were analyzed with administration of short- and long-term FSH imitating androgen deprivation therapy-induced and menopausal FSH elevation. The study showed that short- and long-term exposure of FSH significantly accelerated atherosclerosis progression in apolipoprotein E-deficient mice, manifested as strikingly increased plaques in the aorta and its roots, increased macrophage content, reduced fibrin, and an enlarged necrotic core, suggesting a decrease in plaque stability. Furthermore, expression profiles from the Gene Expression Omnibus GSE21545 dataset revealed that macrophage inflammation was tightly associated with FSH-induced atherosclerotic progression. The human monocyte cell line THP-1 was induced by PMA and worked as a macrophage model to detect inflammatory factors and cellular functions. FSH remarkably promoted the expression of IL-1ß in macrophages and strikingly increased the chemotactic migratory capacity of macrophages toward MCP-1, but the promigratory capacity of FSH was attenuated in foam cells. Overall, we revealed that FSH significantly promoted the inflammatory response and migration of macrophages, thereby provoking atherosclerosis development.
RESUMO
Abnormally high follicle-stimulating hormone (FSH) has been reported to associate with cardiovascular diseases in prostate cancer patients with specific androgen deprivation therapy and in menopausal women. All of the cardiovascular diseases were involved in atherosclerosis. However, the pathogenic mechanism of FSH-associated atherosclerosis remains uncertain. Apolipoprotein E-deficient mice were chosen to develop atherosclerosis, of which the plaques were analyzed with administration of short- and long-term FSH imitating androgen deprivation therapy-induced and menopausal FSH elevation. The study showed that short- and long-term exposure of FSH significantly accelerated atherosclerosis progression in apolipoprotein E-deficient mice, manifested as strikingly increased plaques in the aorta and its roots, increased macrophage content, reduced fibrin, and an enlarged necrotic core, suggesting a decrease in plaque stability. Furthermore, expression profiles from the Gene Expression Omnibus GSE21545 dataset revealed that macrophage inflammation was tightly associated with FSH-induced atherosclerotic progression. The human monocyte cell line THP-1 was induced by PMA and worked as a macrophage model to detect inflammatory factors and cellular functions. FSH remarkably promoted the expression of IL-1ß in macrophages and strikingly increased the chemotactic migratory capacity of macrophages toward MCP-1, but the promigratory capacity of FSH was attenuated in foam cells. Overall, we revealed that FSH significantly promoted the inflammatory response and migration of macrophages, thereby provoking atherosclerosis development.
RESUMO
OBJECTIVE: To compare the difference of therapeutic efficacy of electroacupuncture (EA) stimulation of abdominal acupoints and limb acupoints in the treatment of acute pancreatitis (AP), so as to provide a reference for EA treatment of AP. METHODS: A total of 60 patients with AP were equally and randomly divided into abdominal acupoint group and limb acupoint group. On the basis of retention enema of Chaiqin Chengqi Decoction (containing Radix Bupleurum, Radix Scutellaria, etc.), and abdominal external application of Liuhe Powder ointment (containing Cinnabaris, pearl powder, etc.), patients of the two groups were also treated with acupuncture stimulation of acupoints at the abdomen or limbs. The abdominal acupoints were Shangwan (CV 13), Zhongwan (CV 12), Xiawan(CV 10), Liangmen (ST 21, left), Taiyi(ST 23, left), Chengman (ST 20, left), Fu'ai (SP 16, left), Yindu(KI 19, right), and the limb acupoints were Hegu(LI 4), Neiguan(PC 6), Zusanli(ST 36), Shangjuxu(ST 37), Xiajuxu(ST 39), and Yinlingquan(SP 9) which were punctured with filiform needles by retaining the needles for 30 min after twirling for a while. CV 12 - ST 21, CV 10- SP 16 of the abdomen group, and bilateral PC 6 and ST 36 of the limb group were administered EA (2 Hz/15 Hz, 1 mA and duration of 30 min). The treatment was conducted once daily for 5 days. The abdominal pain severity and distension severity were assessed using the visual analogue scale (VAS), and the abdominal girth was measured by using a soft ruler. RESULTS: Following the treatment, the abdominal pain and distension symptom scores in the lightest and most severe phases of AP and the abdominal girth levels were considerably decreased on the 5th day in the two groups in comparison with their own pre-treatment in the same one group (P 0.05). In addition, no adverse events were found in both groups. CONCLUSION: EA has a good curative effect in the treatment of AP patients. The curative effect of acupuncture of the abdominal acupoints is significantly superior to that of limb acupoints in relieving abdominal pain.
