Unusual 5/5 fused bicyclosesquiterpenoids from Eupatorium adenophorum.

The chemical analysis on the aerial sections of Eupatorium adenophorum Spreng. resulted in the identification of four unprecedented 5/5 fused bicyclosesquiterpenoids, eupatorid A (1), and its analogues named eupatorester A-C (2-4) using various chromatographic techniques. Their structures were unambiguously confirmed by detailed spectroscopic investigations (including 1D, 2D-NMR and HRMS), and single crystal X-ray diffraction. The anti-inflammatory activities, in vitro tumor growth inhibitory activities and antibacterial activities of these compounds were evaluated.

AFG, an important maillard reaction product in red ginseng, alleviates D-galactose-induced brain aging in mice via correcting mitochondrial dysfunction induced by ROS accumulation.

Red ginseng is a classical processed product from Panax ginseng. C.A Meyer with many bioactive components formed through the Maillard reaction called Maillard reaction products. Maillard reaction refers to complex reversible reactions between amino acids or proteins and glycosides, which are used in food processing and storage, as well as in tobacco development, traditional Chinese medicine processing, and wine brewing. Arginyl-fructosyl-glucose (AFG) is a main non-saponin (ginsenoside) component produced in red ginseng processing, with high antioxidant, anti-apoptotic and neuroprotective efficiencies. However, its effects and mechanisms against oxidation stress in on the brain remain elusive. Therefore, this study aimed at exploring the therapeutic effect exerted by AFG on murine subacute brain aging induced by D-galactose (D-gal) and its potential molecular mechanism in the murine model, finding that AFG (40 and 80 mg/kg) significantly ameliorated D-gal-resulted changes in pathology. Besides, according to the transmission electron microscopy (TEM) and Western blot, AFG corrected the mitochondrial dysfunction resulted from ROS, thereby delaying the mice brain aging caused by D-gal.

20(S)-protopanaxatriol inhibited D-galactose-induced brain aging in mice via promoting mitochondrial autophagy flow.

Previous reports have confirmed that saponins (ginsenosides) derived from Panax ginseng. C. A. Meyer exerted obvious memory-enhancing and antiaging effects, and the simpler the structure of ginsenosides, the better the biological activity. In this work, we aimed to explore the therapeutic effect and underlying molecular mechanism of 20(S)-protopanaxatriol (PPT), the aglycone of panaxatriol-type ginsenosides, by establishing D-galactose (D-gal)-induced subacute brain aging model in mice. The results showed that PPT treatment (10 and 20 mg/kg) for 4 weeks could significantly restore the D-gal (800 mg/kg for 8 weeks)-induced impaired memory function, choline dysfunction, and redox system imbalance in mice. Meanwhile, PPT also significantly reduced the histopathological changes caused by D-gal exposure. Moreover, PPT could increase TFEB/LAMP2 protein expression to promote mitochondrial autophagic flow. Importantly, the results from molecular docking showed that PPT had good binding ability with LAMP2 and TFEB, suggesting that TFEB/LAMP2 might play an important role in PPT to alleviate D-gal-caused brain aging.

Jiawei Taohe Chengqi Decoction attenuates hepatic fibrosis by preventing activation of HSCs through regulating Src/ERK/Smad3 signal pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Jiawei Taohe Chengqi Decoction (JTCD) is a Traditional Chinese Medicine (TCM) formula modified from Taohe Chengqi Decoction in the classic ancient literature of TCM "Treatise on Febrile Diseases". Clinical and pharmacological studies have shown that JTCD has a therapeutic effect on hepatic encephalopathy, non-alcoholic fatty liver, cirrhotic ascites, and can alleviate acute liver injury in rats. Our previous studies confirmed that JTCD could alleviate hepatic fibrosis and activation of hepatic stellate cells (HSCs). However, its mechanism remains unclear. AIM OF THE STUDY: This study aimed to elucidate the mechanism of Src Signal on hepatic fibrosis and HSCs activation, and whether JTCD inhibited hepatic fibrosis and HSCs activation through affecting Src Signal. MATERIALS AND METHODS: In vivo, sixty specific pathogen free male C57/BL6 mice were divided into following six groups: Control group, Model group, SARA group, JTCD low dose group, JTCD medium dose group and JTCD high dose group. Then we established a carbon tetrachloride (CCL4)-induced hepatic fibrosis mice model, each JTCD group was given the corresponding dose of JTCD by gavage, the SARA group was given Saracatinib and the control group was given saline, once a day for 4 consecutive weeks. UPLC-Q-TOF-MS analyzed chemical components of JTCD. Pathological examination including Hematoxylin and Eosin (H&E), Masson and Sirius red staining was used to observe the characteristic of hepatic fibrosis. Automatic biochemical analyzer detected the levels of alanine aminotransfease (ALT), and aspartate transaminase (AST) in serum. Western-blot and immunohistochemical staining (IHC) detected protein expression. In vitro, we used shRNA to knock down the expression of Src in immortalized human hepatic stellate cell line (LX-2), then intervened with ERK1/2 agonists/inhibitors and JTCD-containing serum after transforming growth factor ß1 (TGF-ß1) treatment. Immunofluorescence and western-blot detected protein expression. The migratory characteristic of HSCs was assessed by wound-healing assay. RESULTS: We identified 135 chemical components in the water extract of JTCD, and the water extract of JTCD contains a variety of anti-hepatic fibrosis components. Compared to the model group, hepatic fibrosis performance was significantly improved, the serum levels of ALT and AST were significantly decreased in JTCD groups and SARA group, IHC staining and western blot results indicated that JTCD decreased the expressions of α-smooth muscle actin (α-SMA), phospho-Src (Tyr416), phospho-ERK1/2 and phospho-Smad3. In vitro, JTCD-containing serum could significantly decrease the protein expressions of α-SMA, phospho-Src (Tyr416), phospho-ERK1/2 and phospho-Smad3 according to the results of western-blot and immunofluorescence, in addition, JTCD-containing serum inhibited the mobility and activation of LX-2. What's more, after intervening with Src-shRNA, ERK1/2 agonists/inhibitors and JTCD-containing serum, the western-blot results showed that Src/ERK/Smad3 signal has an important role in hepatic fibrosis and HSCs, and JTCD attenuates hepatic fibrosis by preventing activation of HSCs through regulating Src/ERK/Smad3 signal pathway. CONCLUSIONS: The results showed that Src kinase promoted hepatic fibrosis and HSCs activation through the ERK/Smad3 signal pathway. More importantly, the mechanism by which JTCD attenuated hepatic fibrosis and HSCs activation was by inhibiting the Src/ERK/Smad3 signal pathway.

Arginyl-fructosyl-glucose, a major Maillard reaction product of red ginseng mitigates cisplatin-evoked intestinal toxicity in vivo and in vitro.

Cisplatin-evoked profound gastrointestinal symptomatology is one of the most common side effects of chemotherapy drugs, further causing gastrointestinal cell damage, diarrhea and vomiting. Panax ginseng C. A. Meyer, a widely used medicinal and edible plant in China, shows many pharmacological activities. Nevertheless, the role of non-saponin is less known and has great potential in the treatment of severe toxic side effects related to the cisplatin treatment. The present work evaluates the efficiency of a major Maillard reaction product (MRP) of red ginseng, arginyl-fructosyl-glucose (AFG), against cisplatin-evoked intestinal toxicity in vivo and vitro, and the underlying possible mechanisms are also explored. The cisplatin-treated mice (a dose of 20 mg kg-1 for one time) showed serious intestinal mucosa damage accompanied by increased indicators of diamine oxidase (DAO) and decreased expression of tight junction proteins zonula occludens-1 (ZO-1) and occludin. Moreover, cisplatin exposure increased intestinal cell apoptosis with decreased expression of Bcl-2 and increased expression of Bax and cleaved-caspase 3/9 as well as NF-κB related proteins. Interestingly, the supplements of AFG at doses of 40 and 80 mg kg-1 day-1 for 10 days significantly ameliorated these changes. It was also demonstrated in cultured IEC-6 cells that AFG enhanced the expression levels of apoptotic proteins during cisplatin exposure and reduced the sensitivity of IEC-6 cells to cisplatin by inhibiting the activation of GSK3ß and up-regulating the protein expression of ß-catenin. In conclusion, AFG exerted protective effects against cisplatin-induced intestinal toxicity, at least partially by the inhibition of NF-κB-mediated apoptosis, via regulating Wnt/ß-catenin signaling pathway.

Ginsenoside Rg5: A Review of Anticancer and Neuroprotection with Network Pharmacology Approach.

Ginsenoside Rg5 (G-Rg5) is a rare ginsenoside isolated from ginseng (Panax ginseng C.A. Meyer), and this compound is increasingly known for its potent pharmacological activities. This study aimed to provide a comprehensive review of the main activities and mechanisms of G-Rg5 by adopting network pharmacological analysis combined with a summary of published articles. The 100 target genes of G-Rg5 were searched through available database, subjected to protein-protein interaction (PPI) network generation and then core screening. The results showed that G-Rg5 has promising anticancer and neuroprotective effects. By summarizing these two pharmacological activities, we found that G-Rg5 exerts its therapeutic effects mainly through PI3K/AKT, MAPK signaling pathways, and the regulation of apoptosis and cell cycle. And these results were corroborated by KEGG analysis. Likewise, molecular docking of the related proteins was performed, and the binding energies were all less than [Formula: see text]7.0[Formula: see text]kJ/mol, indicating that these proteins had excellent binding capacity with G-Rg5. The network pharmacology results revealed many potential G-Rg5 mechanisms, which need to be further explored. We expect that the network pharmacology approach and molecular docking techniques can help us gain a deeper understanding of the therapeutic mechanisms of different ginsenosides and even the ginseng plant, for further developing their therapeutic potential as well as clinical applications.

Evaluating the effects of mitochondrial autophagy flux on ginsenoside Rg2 for delaying D-galactose induced brain aging in mice.

BACKGROUND: Aging is an inevitable gradual process of the body, which can cause dysfunction or degeneration of the nervous or immune system, thus becoming a critical pathogenic factor inducing neurodegenerative diseases. Previous reports have confirmed that saponins (ginsenosides) derived from Panax ginseng. C.A. Meyer exerted obvious memory-enhancing and anti-aging effects, and the simpler the structure of ginsenosides, the better the biological activity. Ginsenoside Rg2 (Rg2) is a prominent and representative panaxatriol-type ginsenoside produced during ginseng processing, which has been reported to have pretty good neuroprotective activity. PURPOSE: The work was aimed at exploring the therapeutic effects and possible molecular mechanisms of Rg2 by establishing the subacute brain aging model induced by D-galactose (D-gal) in mice. METHODS: The anti-aging activity of G-Rg2 (10, 20 mg/kg for 4 weeks) was assessed using the D-gal induced brain aging model (800 mg/kg for 8 weeks). The Morris water maze (MWM) and histopathological analysis were used to evaluate the cognitive function and pathological changes of the brain in mice, respectively. The protein expression levels of p53, p21, p16ink4α, IL-6, CDK4, ATG3, ATG5, ATG7, LC3, p62, LAMP2, and TFEB were quantified through western blot analysis. The degree of mitochondrial damage and the number of mitochondrial autophagolysosomes in hippocampal neurons were monitored using TEM analysis. RESULTS: The results showed that Rg2 could significantly restore D-gal-induced impaired memory function, choline dysfunction, and redox system imbalance in mice. Rg2 treatment also considerably decreased the over-expression of aging-related proteins such as p53/p21/p16ink4α induced by D-galactose, which demonstrated that Rg2 possessed good anti-aging activity. Meanwhile, Rg2 could evidently reduce the pathological changes caused by D-gal exposure. Moreover, the results from transmission electron microscopy and western blot analysis indicated that Rg2 could delay the brain aging induced by D-gal in mice via promoting the degradation of the autophagy substrate p62 while increasing the protein expression level of LAMP2/TFEB to maintain mitochondrial function. CONCLUSION: These results indicate that Rg2 could postpone brain aging by increasing mitochondrial autophagy flux to maintain mitochondrial function, which greatly enriched the research on the pharmacological activity of ginsenosides for delaying brain aging.

Protective Effect of Ginsenosides from Stems and Leaves of Panax ginseng against Scopolamine-Induced Memory Damage via Multiple Molecular Mechanisms.

Although growing evidence has shown that ginsenosides from stems and leaves of Panax ginseng (GSLS) exercise a protective impact on the central nervous system, in the model of memory damage induced by scopolamine, it is still rarely reported. Thus, the mechanism of action needs to be further explored. This study was to investigate the effect of GSLS on scopolamine (SCOP)-induced memory damage and the underlying mechanism. Male ICR mice were treated with SCOP (3 mg/kg) for 7 days, with or without GSLS (75 and 150 mg/kg) treatment for 14 days. After GSLS treatment, the memory damage induced by SCOP was significantly ameliorated as shown by the improvement of cholinergic function (AChE and ChAT), brain tissue hippocampus morphology (H&E staining), and oxidative stress (MDA, GSH, and NO). Meanwhile, immunohistochemical assay suggested that GSLS increased the expression of brain-derived neurotrophic factor (BDNF) and Tyrosine Kinase receptor B (TrkB). Further mechanism research indicated that GSLS inhibited the Tau hyperphosphorylation and cell apoptosis by regulating the PI3K/AKT pathway and inhibited neuroinflammation by regulating the NF-κB pathway, thereby exerting a cognitive impairment improvement effect. This work suggested that GSLS could protect against SCOP-induced memory defects possibly through inhibiting oxidative stress, inhibiting neuroinflammation and cell apoptosis.

Protective Effect of 20(R)-Ginsenoside Rg3 Against Cisplatin-Induced Renal Toxicity via PI3K/AKT and NF-[Formula: see text]B Signaling Pathways Based on the Premise of Ensuring Anticancer Effect.

Although the protective effect of ginsenoside on cisplatin-induced renal injury has been extensively studied, whether ginsenoside interferes with the antitumor effect of cisplatin has not been confirmed. In this paper, we verified the main molecular mechanism of 20(R)-ginsenoside Rg3 (R-Rg3) antagonizing cisplatin-induced acute kidney injury (AKI) through the combination of in vivo and in vitro models. It is worth mentioning that the two cell models of HK-2 and HepG2 were used simultaneously for the first time to explore the effect of the activation site of tumor-associated protein p53 on apoptosis and tumor suppression. The results showed that a single injection of cisplatin (20 mg/kg) led to weight loss, the kidney index of the mice increased, and creatinine (CRE) and blood urea nitrogen (BUN) levels in mice sharply increased. Continuous administration of R-Rg3 at doses of 10 and 20 mg/kg for 10 days could significantly alleviate this symptom. Similarly, R-Rg3 treatment reduced oxidative stress damage caused by cisplatin. Moreover, R-Rg3 could observably reduce the apoptosis and inflammatory infiltration of renal tubular cells induced by cisplatin. We used western blotting analysis to demonstrate that R-Rg3 restored cisplatin-induced AKI might be related to PI3K/AKT and NF-[Formula: see text]B mediated apoptosis and inflammation pathways. In the meantime, we also verified that R-Rg3 could activate different sites of p53 to control renal cell apoptosis induced by cisplatin without affecting its antitumor effect.

Red ginseng protects against cisplatin-induced intestinal toxicity by inhibiting apoptosis and autophagy via the PI3K/AKT and MAPK signaling pathways.

Although growing evidence has shown that ginseng (Panax ginseng C.A. Meyer.) exerts strong protective and preventive effects on cisplatin-induced side effects, including nephrotoxicity, ototoxicity and cardiotoxicity, the ameliorative effects of ginseng on intestinal damage caused by cisplatin are unknown to date. Red ginseng (RG), a major processed product of the roots of Panax ginseng C.A. Meyer, can be used to control chemotherapy drug-induced multiple toxicity. In the present work, an animal model of cisplatin-induced intestinal injury was established to evaluate the ameliorative effects of RG and their underlying molecular mechanism for the first time. The results showed that a single cisplatin injection (20 mg kg-1) leads to loss of body weight, shrinkage of the small intestine, and sharp increase of the intestinal function index of diamine oxidase (DAO). These symptoms were remarkably relieved after the administration of RG at 300 and 600 mg kg-1 for 10 continuous days, respectively. In addition, RG markedly reduced the increase in malondialdehyde (MDA) levels and the consumption of superoxide dismutase (SOD) and catalase (CAT) caused by cisplatin-induced oxidative stress. Furthermore, RG pretreatment dramatically improved the cisplatin-induced apoptosis of intestinal villous cells, irregular nuclear arrangement, ablation of crypt cells, and damage to the mechanical barrier. In this study, pharmacological methods have been used to prove that RG can inhibit cisplatin intestinal toxicity by activating the PI3K/AKT signaling pathway to inhibit apoptosis and by antagonizing the MAPK-mediated autophagy pathway.

[Post-stroke hand spasm treated with penetrating acupuncture combined with kinesiotherapy: a randomized controlled trial].

OBJECTIVE: To compare the differences in the clinical effect on post-stroke hand spasm among the combined treatment of penetrating acupuncture and kinesiotherapy, the simple application of penetrating acupuncture and the simple application of kinesiotherapy. METHODS: A total of 105 patients with post-stroke hand spasm were randomized into a penetrating acupuncture group, a kinesiotherapy group and a combined treatment group, 35 cases in each one, of which, 2 cases were dropped out in either the combined treatment group and the penetrating acupuncture group, and 1 case dropped out in the kinesiotherapy group. The routine rehabilitation training, e.g. occupational therapy and Bobath exercise and medication were adopted in all of the three groups. In the penetrating acupuncture group, the penetrating needling technique was exerted from Hegu (LI 4) to Houxi (SI 3) and from Waiguan (TE 5) to Sidu (TE 9) on the affected side. In the kinesiotherapy group, the persistent movement or passive movement was exerted on the wrist joint, the metacarpophalangeal joints and the interphalangeal joints. In the combined treatment group, the penetrating acupuncture (the same as the penetrating acupuncture group) was exerted combined with kinesiotherapy (the same as the kinesiotherapy group). In each group, the treatment was given once a day, 30 min in each time, 6 treatments a week in total, with the interval of 1 day between the courses. The treatment for 2 weeks was as one course and 2 courses were required totally. Before and after treatment, the scores of hand spasm index, hand-wrist motor function and the activity of daily living (ADL) were compared in each group. RESULTS: After treatment, the scores of hand spasm index were reduced as compared with those before treatment in each group (P<0.05) and the scores of hand-wrist motor function and ADL were increased significantly as compared with those before treatment in each group (P<0.05). After treatment, the reducing degree of the score of hand spasm index in the combined treatment group was greater than the penetrating acupuncture group and the kinesiotherapy group (P<0.01), and the increasing degree of the scores of hand-wrist motor function and ADL were higher than either the penetrating acupuncture group or the kinesiotherapy group (P<0.01). The improvements in each index were not different statistically between the kinesiotherapy group and the penetrating acupuncture group (P>0.05). CONCLUSION: Compared with the simple application of either penetrating acupuncture or kinesiotherapy, the combined treatment of them achieves the significant improvements in hand spasm degree, hand wrist motor function and ADL in patients with stroke.

Metabolic profiling of RB-2 and RB-4, two analogs of polyacetylene from Bupleurum.

RB-2 and RB-4 are two structural analogs of polyacetylene from Radix Bupleuri that show antidepressant effects. However, no metabolic data are available to elucidate their systemic homeostasis. Mass spectrometry combined with liver microsomes and recombinant drug-metabolizing enzymes were performed to profile the biotransformations of RB-2/RB-4 in vitro and in vivo. Oxidation should be the major metabolic pathways for them in phase I, while CYP2C9 and CYP2E1 was the major contributor. In phase II, conjugational groups usually combined with the metabolites from phase I. This study provides an important reference basis for the safety evaluation and rational application of RB-2/RB-4.

Effect of alternate-day fasting therapy combined with Linggui Zhugan Decoction () on hepatic oxidative stress in hyperlipidemic rat.

OBJECTIVE: To observe the effect of alternate-day fasting (ADF) therapy combined with Linggui Zhugan Decoction (, LZD) on hepatic oxidative stress and blood lipids in hyperlipidemic rats. METHODS: Fifty-two Wistar rats were randomly assigned to two groups: the high-fat-diet (HF) group and the normal-diet (ND) group. Hyperlipidemia was induced by feeding rats with high-cholesterol-diet for 5 weeks. Then the HF group was randomized to the model-control (MC) group, the alternate-day-fasting (ADF) group, and the ADF combined with LZD (AL) group. The ND group was regarded as the negative control (NC) group. The AL and ADF groups were put on fast for 24 h on alternate days for 4 weeks. The AL group was administrated with LZD on the fast days. Body weight and food intake were measured once a week. After 4-week ADF, blood sample was collected for determination of plasma total cholesterol (TC), triglyceride (TG), low-density-lipoprotein cholesterol (LDL-C) and high-density-lipoprotein cholesterol (HDL-C). Liver oxidative stress parameters including total superoxide dismutase (T-SOD) activity, malondialdehyde (MDA) level and glutathione (GSH) content were also tested. RESULTS: Body weight in the HF group decreased significantly (P<0.01). TC, TG, HDL-C, and LDL-C concentrations in the HF group were higher than those in the NC group (P<0.01), respectively. T-SOD in the HF group was clearly lower than that in the NC group (P<0.05). After 4-week intervention, body weight, TC and TG concentrations in the ADF and AL groups declined significantly, respectively, compared to MC group (P<0.05). GSH in the ADF and AL groups were much higher than those in the MC group (P<0.01). MDA level was also greatly higher in the ADF group as compared with the NC group (P<0.05). CONCLUSION: ADF therapy combined with LZD may be used as an effective combination approach for treatment of hyperlipidemia and oxidative stress damage.

An uncommon plant growth regulator, diethyl aminoethyl hexanoate, is highly effective in tissue cultures of the important medicinal plant purple coneflower (Echinacea purpurea L.).

We investigated the effects of various concentrations of diethyl aminoethyl hexanoate (DA-6) on the regeneration and growth of adventitious buds in in vitro purple coneflower cultures. Among the 3 types of explants tested, leaf explants required higher concentrations of DA-6 than petiole and root explants in order to obtain high regeneration rates, while root explants required the lowest concentration of DA-6. Additionally, explants with higher ploidy levels were more sensitive to the addition of DA-6, while explants with lower ploidy levels required higher concentrations of DA-6 to achieve its maximal regeneration rate. Interestingly, the application of a concentration that was conducive to the regeneration of explants with lower ploidy levels was inhibitory to the regeneration of explants with higher ploidy levels. Moreover, during the growth of regenerated buds, DA-6 application significantly improved plant height and weight, root weight, root thickness, root number, primary root length, total root length, and root/top ratio. Differences in the responses of explants to supplementation with DA-6 were also observed among explants with different ploidy levels, with buds having lower ploidy levels responding to lower concentrations of DA-6. Taken together, the results of the present experiments showed that proper application of DA-6 could increase in vitro culture efficiency in purple coneflower.

Effects of the modified linggui zhugan decoction (see text) combined with short-term very low calorie diets on glycemic control in newly diagnosed type 2 diabetics.

OBJECTIVE: To evaluate the effects of the modified Linggui Zhugan Decoction (see text) combined with short-term very low calorie diets (VLCDs) on glycemic control in newly diagnosed type 2 diabetes mellitus (T2DM) patients. METHODS: A total of 20 subjects with newly diagnosed T2DM were treated with the modified Linggui Zhugan Decoction (one-month administration) combined with short-term VLCDs (5 days), and 3-months follow-up. A standard 75-g oral-glucose-tolerance test (OGTT) indexes fasting plasma glucose (FPG), post-prandial 0.5 h and 2 h plasma glucose (P0.5hPG, P2hPG), glycated hemoglobin A(1c) (GHbA(1c)), body weight, body mass index (BMI), insulin function, insulin resistance index, incidence of hypoglycemia, and the liver and renal functions were evaluated before and after treatment. Correlations of BMI with insulin function and insulin resistance were also assessed. RESULTS: After the treatment, the patients' plasma glucose decreased steadily, FPG decreased from 5.8 +/- 0.9 mmol/L at pre-treatment to 5.0 +/- 0.6 mmol/L at 3-months follow-up (P < 0.05), and P2hPG decreased from 11.7 +/- 3.8 mmol/L at pre-treatment to 6.9 +/- 0.9 mmol/L at 3-months follow-up (P < 0.01). The level of GHbA(1c) declined from (6.47 +/- 1.24)% at pre-treatment to (6.14 +/- 0.99)% at 3-months follow-up (P < 0.01). Body weight and BMI also declined significantly. Insulin resistance index was improved obviously and no event of hypoglycemia occurred. Part of the patients companied with fatty liver had a transient increase in hepatic transaminase during the treatment, but it turned to normal after the treatment. CONCLUSIONS: The modified Linggui Zhugan Decoction combined with short-term VLCDs can be safely implemented for steady glycemic control in newly diagnosed T2DM patients.

[Effect of acupoint-catgut implantation on the physical agility of professional athletes].

OBJECTIVES: To observe the impact of acupoint-catgut implantation on physical agility of athletes and to probe into its underlying mechanism. METHODS: A total of 68 volunteer athletes were recruited in the present study. Sixteen rowers of China National Women's Racing Boat Team (CNWRBT) underwent comparative observation between pre- and post-treatment with acupoint-catgut implantation. Fifty-two athletes from Zhejiang Heavy Athletics Events Team (HAET) and Sand-beach Volleyball Team (SBVT) were randomized into control (n = 26) and treatment (n = 26) groups which were treated with massage (20 mm, once daily for 1 year), and catgut implantation at Guanyuan (CV 4), Mingmen (GV 4), etc. (once every two weeks), respectively. In the later group, after 6 times of treatment, the catgut implantation was given once a month, continuously for 1 year. Serum testosterone and plasma hemoglobin (Hb) levels were detected before, 1.5 mon, 3 mon, 6 mon and 12 mon after the treatment, respectively. RESULTS: 1) Compared with pre-treatment, the 2 000 m ergometer time was shortened significantly (P < 0.01), and serum testosterone and plasma hemoglobin (Hb) levels were increased evidently in 16 volunteer rowers of CNWRBT after 3 months' acupoint-catgut implantation treatment (P < 0.05, P < 0.01). 2) In comparison with control group and pre-treatment, the midium- and long-distance running scores of the athletes of Zhejiang HAET and SBVT were elevated considerably (P < 0.01), serum testosterone and plasma Hb levels increased significantly (P < 0.05). CONCLUSION: Acupoint-catgut implantation can significantly improve the athletes' anti-fatigue exercise capacity, enhance their physical agility to elevate their athletics events score, which may be closely related to its effects in raising blood testosterone and hemoglobin levels.