Research Trends of Acupuncture Therapy on Chronic Pelvic Pain Syndrome from 2000 to 2022: A Bibliometric Analysis.

Background: Acupuncture is considered an important means of analgesic, which has been widely used in chronic pelvic pain syndrome (CPPS) management and treatment in recent years, published a large number of related documents. However, the relevant literature in this field has not been summarized and quantitatively analyzed. Therefore, this study aims to analyze the hotspots and predicting future research trends of acupuncture on pelvic pain syndrome. Methods: Search for the relevant publications of the web of science database from 2000 to 2022 about the treatment of acupuncture on chronic pelvic pain syndrome. The Citespace software and VosViewer software are used to analyze the visualization of the countries, institutions, authors, keywords and references and references in the literature. Results: A total of 173 publications were included. The annual number of essays gradually showed an overall growth trend over time. Medicine magazine is the most published journal in this field. J UROLOGY and Acupunct Med are the most cited journals and the most influential magazines; The most active and influential country is China, and the most produced institutions are Beijing University of Chinese Medicine; The most produced authors are Liu Zhishun. The most cited and most influential authors are Nickel JC and Armour M; keywords and cited reference analysis show that the quality of life, mechanism research, alternative medicine and electro-acupuncture will be the scientific hotspot of acupuncture treatment for chronic pelvic pain syndrome. Conclusion: This study shows that acupuncture on CPPS is increasingly valued and recognized. The future research hotspots will focus on the effects and mechanisms. In the future, more high-quality animal basic research will be required to explore the exact mechanism of acupuncture on CPPS. In addition, different parameters of acupuncture such as electric-acupuncture, stimulating frequency, duration and strength are also the focus of future research. More clinical trials are required to verify its safety and effectiveness.

Improved fatigue properties, bone microstructure and blood glucose in type 2 diabetic rats with verapamil treatment.

BACKGROUND: Type 2 diabetes mellitus is a global epidemic disease, which leads to a severe complication named increased bone fracture risk. This study aimed to explore if verapamil treatment could improve bone quality of type 2 diabetes mellitus. METHODS: Rat models of control, diabetes and verapamil treatment with 4/12/24/48 mg/kg/d were established, respectively. Blood glucose was monitored during 12-week treatment, and bilateral tibiae were collected. Microstructural images of bilateral metaphyseal cancellous bone and high-resolution images of cortical bone of left tibial shafts were obtained by micro-computed tomography. Fatigue properties of bone were evaluated via cyclic compressive tests of right tibial shafts. FINDINGS: Verapamil treatment had no significant effect on blood glucose, but blood glucose tended to decline with the increase of verapamil-treated time and dose. Compared with controls, osteocyte lacunar and canal porosities in diabetes and verapamil-treated groups were significantly decreased (P < 0.05), trabecular separation and degree of anisotropy were significantly increased (P < 0.05), while trabecular tissue mineral density, trabecular bone volume fraction and trabecular number in verapamil-treated (48 mg/kg/d) group were significantly higher than those in diabetes (P < 0.05). Compared with diabetes, initial compressive elastic moduli in verapamil-treated (12/24/48 mg/kg/d) groups were significantly increased (P < 0.05), while secant modulus degradations in verapamil-treated (24/48 mg/kg/d) groups were significantly decreased (P < 0.05). INTERPRETATION: Verapamil could improve bone microstructure and fatigue properties in type 2 diabetic rats; and high-dose verapamil presented a significant effect on improving bone quality. These findings provided a new possibility for preventing the high bone fracture risk of type 2 diabetes mellitus in clinics.

Short-term pretreatment of naringin isolated from Citrus wilsonii Tanaka attenuates rat myocardial ischemia/reperfusion injury.

Pretreatment or treatment with anti-apoptotic, anti-inflammatory, or anti-oxidative approaches could be critical for attenuated the severity of myocardial ischemia/reperfusion (I/R) injury. Naringin, a natural flavonoid, plays important roles in inflammation-related diseases. Immature dry fruits of Citrus wilsonii Tanaka (Xiang Yuan) are rich in naringin that can be used as traditional Chinese medicine to treat inflammation-related symptoms. However, its roles in cardioprotective role remain unclear. This study aimed to isolate naringin from Citrus wilsonii Tanaka fruit and tested their cardioprotective effect. The dry fruits of Citrus wilsonii Tanaka were extracted with boiling water and then supernatants were freeze-dried to yield aqueous extract (ZQAE). The extract was chemoprofiled using UPLC-MS/MS to stand for major constituents, and then subjected to different chromatographic separation steps, and naringin was isolated in a high yield. The cardioprotective effects of the aqueous extract of ZQAE and naringin were investigated in a myocardial I/R rat model and to elucidate the mechanism underlying its cardioprotective effect. Our results indicated that 5-day ZQAE and naringin pretreatments both promoted histopathological changes and reduced myocardial enzymes (cTnl, CK-MB, CK and LDH) induced by I/R. Moreover, the 50 mg/kg and 100 mg/kg ZQAE dose pretreatments presented a significantly decreased infarct size as well as myocardial enzyme levels but also inhibited myocardial apoptosis (cleaved-caspase3 protein expression), the inflammatory response (IL-23, IL-6, and TNF-α) and oxidative stress (MDA and SOD). The cardioprotective effect of 5 mg/kg dose of naringin pretreatment is comparable with that of 5 mg/kg drug ditiazem pretreatment. Additionally, naringin pretreatment exhibited striking decreases in the apoptosis index and downregulation of the protein expression levels of cleaved-Caspase3, Bcl2 and Bax. Meanwhile, naringin downregulated HMGB1 expression and upregulated SIRT1 expression in the myocardium. These findings suggest that short-term pretreatments with ZQAE and naringin both protect against myocardial I/R injury by suppressing myocardial apoptosis, the inflammatory response, and oxidative stress. The cardioprotective effect of naringin involves SIRT1 activation and may interact with HMGB1 and inhibit the release of HMGB1.

Effects of tanshinone IIA on fibrosis in a rat model of cirrhosis through heme oxygenase-1, inflammation, oxidative stress and apoptosis.

Tanshinone IIA is extracted from the root of Salvia miltiorrhiza and used in traditional Chinese medicine for its anti-inflammatory activity and antioxidant effects. The aim of the present study was to investigate the potential protective effects of tanshinone IIA against fibrosis in a rat model of cirrhosis and to elucidate the underlying mechanisms. Male Sprague Dawley rats were used as the model of cirrhosis in the present study. In the cirrhotic rats, the extent of fibrosis, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), heme oxygenase­1 (HO­1) protein expression, serum levels of nuclear factor (NF)­κB, tumor necrosis factor­α (TNF­α), interleukin (IL)­1ß and IL­6, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH­PX), and the protein expression levels of phosphorylated­p38 mitogen­activated protein kinase (MAPK) were all significantly increased. However, the serum malondialdehyde (MDA) activity and protein kinase B (Akt) protein expression were suppressed in cirrhotic rats compared with the sham (control) group. Compared with the cirrhotic group, administration of tanshinone IIA reduced the extent of fibrosis, levels of ALT and AST, HO­1 protein expression, serum NF­κB, TNF­α, IL­1ß and IL­6 levels, and the activity of SOD, CAT and GSH­PX. Furthermore, administration of tanshinone IIA significantly increased the inhibition of the serum MDA activity and the Akt protein expression in cirrhotic rats compared with those in the cirrhotic group. The protective effect of tanshinone IIA suppresses fibrosis in a rat model of cirrhosis, and reduces inflammation and oxidative stress, via the HO­1, Akt and p38 MAPK signaling pathway.

Curcumin Attenuates Hydrogen Peroxide-Induced Premature Senescence via the Activation of SIRT1 in Human Umbilical Vein Endothelial Cells.

Endothelial senescence has been proposed to be involved in endothelial dysfunction and atherogenesis. Curcumin, a natural phenol, possesses antioxidant and anti-inflammatory properties. However, the effect of curcumin on endothelial senescence is unclear. This study explores the effect of curcumin on hydrogen peroxide (H2O2)-induced endothelial premature senescence and the mechanisms involved. Human umbilical vein endothelial cells (HUVECs) were cultured, and premature senescence was induced with 100 µM H2O2. Results showed that pretreatment with curcumin significantly attenuated the H2O2-induced HUVECs' premature senescence, which was evidenced by a decreased percentage of senescence-associated ß-galactosidase positive cells, improved cell division and decreased expression of senescence-associated protein p21 (all p<0.05). Pretreatment with curcumin decreased oxidative stress and apoptosis in H2O2-treated HUVECs. Treatment of HUVECs with H2O2 also down-regulated the phosphorylation of endothelial nitric oxide synthase (eNOS), decreased the level of nitric oxide in the culture medium, and inhibited the protein expression and enzymatic activity of silent information regulator 1 (SIRT1), while pretreatment with curcumin partly reversed these effects (all p<0.05). Treatment with curcumin alone enhanced the enzymatic activity of SIRT1, but didn't affect cellular senescence, cell growth or apoptosis compared to the Control. The inhibition of SIRT1 using SIRT1 short interfering RNA (siRNA) could decrease the expression and phosphorylation of eNOS and abrogate the protective effect of curcumin on H2O2-induced premature senescence. These findings suggest that curcumin could attenuate oxidative stress-induced HUVECs' premature senescence via the activation of SIRT1.

Moxa-stick suffumigation for disinfecting air in hematology and hematopoietic stem cell transplantation wards with class 100 laminar flow.

OBJECTIVE: To evaluate the effect of moxa-stick suffumigation in the hematology and hematopoietic stem cell transplantation (HSCT) wards with luminar flow. METHODS: The plate exposure method was used to measure the effect of air-disinfection of moxa-stick suffumigation in hematology and HSCT wards. The yearly average qualified rates of air sampling in HSCT wards were evaluated from 2007 to 2010. To further investigate the disinfecting effect of moxa-stick suffumigation, the colony counts of common pathogens (including Staphylcoccus aureus and Pseudomonas aeruginosa) before and after moxa-stick suffumigation were compared. RESULTS: The mean air quality rates of the HSCT wards with class 100 laminar flow were all above 90.0% (91.2%-96.2%) from 2007 to 2010. Moxa-stick suffumigation effectively decreased the presence of bacteria in the hematology ward's air (P<0.01). The most notable effect was the drastic reduction in the colony counts of Staphylococcus aureus and Pseudomonas aeruginosa on the blood plates exposed to air treated with moxa-stick suffumigation (77.1±52.9 cfu/m(2) vs 196.1±87.5 cfu/m(2), P<0.01; and 100.2±35.3 cfu/m(2) vs 371.5±35.3 cfu/m(2), P<0.01). CONCLUSION: Moxa-stick suffumigation proved to be a reliable and effective airdisinfection method for hematology and HSCT wards, and hence, it should be employed extensively.

[Study on binding forms of selenium in selenium-enriched Salvia miltiorrhiza].

OBJECTIVE: To understand the absolute and relative concentrations of proteins,polysaccharides and nucleic acids that are Selenium-binding in Selenium-enriched Salvia miltiorrhiza, and to determine the efficiency of biotransformation of inorganic Selenium compounds in Salvia miltiorrhiza. METHODS: Extract the Selenium-binding proteins, polysaccharides and nucleic acids in Selenium-enriched Salvia miltiorrhiza using different solvents. Determine the concentrations of proteins, polysaccharides and nucleic acids by spectrophotometry, the concentration of Selenium by Hydride generation atomic fluorescence spectrometry. RESULTS: Selenium-binding proteins took up 74.2% of the total amount of Selenium in the tested Salvia miltiorrhiza, while Selenium-binding polysaccharides took up 39.5% and Selenium-binding nucleic acids took up 2.3%. Selenium that was bound with the water-soluble proteins came out as the most con- centrated, taking up 46.0% of the total amount of Selenium, during the extraction of Selenium using water, NaCl, ethanol and NaOH solution, respectively. Being extracted by the weak acid and alkali phosphoric acid buffer solutions, Selenium-binding proteins were more concentrated in the alkali buffer solution, taking up 51.2% of the total amount. CONCLUSIONS: In Salvia miltiorrhiza, Selenium exists mainly in the forms of selenium-binding proteins and Selenium-binding polysaccharides. Cultivation of Selenium-enriched Salvia miltiorrhiza achieves the biotransformation of inorganic Selenium compounds into organic compounds efficiently.

Naringenin inhibits angiotensin II-induced vascular smooth muscle cells proliferation and migration and decreases neointimal hyperplasia in balloon injured rat carotid arteries through suppressing oxidative stress.

Proliferation and migration of vascular smooth muscle cells (VSMCs) play pivotal roles in the development of restenosis after angioplasty and oxidative stress involves both processes. Naringenin, a flavanone compound found in citrus fruits, has been widely evaluated for antioxidant activity. This study was designed to explore whether naringenin could inhibit angiotensin II-induced VSMCs proliferation and migration and decrease neointimal hyperplasia in balloon injured rat carotid arteries. VSMCs were treated with or without naringenin before stimulation with 1 µM angiotensin II and twenty-four rats were subjected to carotid arteries injury and the carotid arteries were harvested at 14 d after balloon injury. The results showed naringenin led to a significant inhibition of angiotensin II-induced VSMCs proliferation and migration. Naringenin significantly attenuated the reactive oxygen species production, increased the superoxide dismutase activity and decreased the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, reduced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) and the nuclear translocation of nuclear factor (NF)-κB p65 in angiotensin II-treated VSMCs. Moreover, naringenin decreased the ratio of neointima to media by 63.8% in balloon injured rat carotid arteries, and the serum level of 8-iso-prostaglandin F2α in naringenin-treated rats was significantly decreased. These results indicated naringenin exhibited antioxidant activity on angiotensin II-treated VSMCs and balloon injured rat carotid arteries and could be a potential protective agent for restenosis after angioplasty.

Effects of low-intensity atrial ganglionated plexi stimulation on ventricular electrophysiology and arrhythmogenesis.

BACKGROUND: Atrial ganglionated plexi (GP) have been shown to modulate sinus rate, atrioventricular conduction and atrial electrophysiology. The aim of this study was to investigate the effect of low-intensity GP stimulation (GPS) on ventricular electrophysiological properties in normal heart and on ventricular arrhythmogenesis after acute myocardial ischemia (AMI) in canine. METHODS AND RESULTS: Thirty-nine dogs were assigned into the normal heart group (n=12) and the acute myocardial ischemia (AMI) group (n=27, 12 in control and 15 in low-intensity GPS). In the normal heart group, ventricular effective refractory period (ERP), dynamic restitution and electrical alternans were measured at baseline and after 6-hour low-intensity GPS. In the AMI group, the incidence of ventricular arrhythmias was determined during 1-hour recording after AMI was induced. In the normal heart, 6-hour low-intensity GPS significantly prolonged ventricular ERP and action potential duration (APD) at each site (all P<0.05) but did not change their spatial dispersions when compared with baseline. Low-intensity GPS also caused an upward shift of ventricular restitution curves in each site but did not change the slope of restitution curves. APD alternans after low-intensity GPS occurred at longer pacing cycle length at each site when compared with baseline (all P<0.05). In the AMI heart, the incidence of ventricular arrhythmias in low-intensity GPS group was significantly lower than that in control group (P<0.05). CONCLUSIONS: Low-intensity GPS induces no increase in the risk of ventricular arrhythmias in the normal heart as well as protects against ventricular arrhythmogenesis during AMI.

Low-level ganglionated plexus stimulation facilitates atrial fibrillation: in vivo and in vitro studies.

OBJECTIVES: The purpose of the present study was to investigate whether long term low level autonomic activation can form electrophysiological substrate for atrial fibrillation (AF). METHODS AND RESULTS: In 16 anesthetized open-chest dogs, electrodes on the anterior right ganglionated plexuses (GP) and superior left GP allowed 6-h low-level GP stimulation (LL-GPS) inducing a 10% decrease in sinus rate. Similar low-level stimulation (without myocardial capture) was delivered to the myocardium remote from the GP for 6h in another 16 dogs as control group. LL-GPS: a) induced shortening of the atrial effective refractory period and increase of the window of vulnerability for AF; b) significantly increased acetylcholine-regulated potassium current (I(KACh)) at left superior pulmonary vein (LSPV) while reduced the density of L-type calcium current (I(CaL)) at LSPV and both atria, the protein expression of the channel subunit showed a consistent alteration, however both without significant changes in mRNA level. CONCLUSIONS: Six-hour LL-GPS induced significant changes in atrial electrophysiology and facilitated the initiation of AF, indicating that long-term low level autonomic activation would form electrophysiological substrate for AF. The underlying mechanism may be associated with a post-transcriptional regulation of increased I(KACh) and decreased I(CaL).

[Determination of mercury and selenium in bone by atomic absorption spectrometry after microwave digestion].

Mercury and selenium in the rats' thighbone were determinated by cold atom absorbance and flow injection hydride atom absorbance after digesting by microwave. The method of sample's making and digesting was discussed. The factors of determination of selenium were studied. The detection limits of mercury and selenium are 1.65 and 1.78 ng x mL(-1) respectively. The RSD% of mercury and selenium are 4.1% and 3.6% respectively. The linearity of calibration curve of mercury and selenium are in the concentrations of 0-120 ng x mL(-1) and 0-50 ng x mL(-1) respectively. The recovery of mercury and selenium are 93.72%-101.8% and 95.53%-102.2% respectively.

[Determination of selenium in rat's organs by graphite microwave dissolution].

The content of selenium in rat's ten organs was determined by graphite furnace atomic absorption spectrometry with microwave dissolution. Inorganic palladium modifier was added into the sample to solve the problems of selenium volatilization and matrix disturbance as selenium in the sample is liable to receive serious loss during the course of digestion and cineration. The optimistic determination conditions were shown as follow, digestion reagent of 4 mL (10:3)HNO3/H2O2, matrix modification of 50 microg x mL(-1) palladium chloride, cineration temperature of 1200 degrees C and atomization temperature of 1800 degrees C. Under such optimum conditions, the linear range is 0-80 ng x mL(-1) and the detection limit is 1.83 ng x mL(-1). The RSD is less than 8% and the average recovery rate is 97.6%. The method was shown to be precise, reliable, convenient and quick in selenium determination of various organism organs.