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The new progress has been made in the research of programmed cell death (e.g. autophagy, apoptosis, pyroptosis, necroptosis and ferroptosis) for the pathological mechanism of ischemic stroke. As an important non-pharmacological therapy, acupuncture is widely used in stroke patients and has achieved favorable effect. The researches in recent years have shown that acupuncture plays its neuroprotective role on ischemic stroke by modulation of autophagy, apoptosis, pyroptosis, necroptosis and ferroptosis of neurons. Acupuncture is effective in treatment of ischemic stroke by regulating programmed cell death.

To study the residue and dietary risk of propiconazole in Panax notoginseng and the effects on physiological and bioche-mical properties of P. notoginseng, we conducted foliar spraying of propiconazole on P. notoginseng in pot experiments. The physiolo-gical and biochemical properties studied included leaf damage, osmoregulatory substance content, antioxidant enzyme system, non-enzymatic system, and saponin content in the main root. The results showed that at the same application concentration, the residual amount of propiconazole in each part of P. notoginseng increased with the increase in the times of application and decreased with the extension of harvest interval. After one-time application of propiconazole according to the recommended dose(132 g·hm~(-2)) for P. ginseng, the half-life was 11.37-13.67 days. After 1-2 times of application in P. notoginseng, propiconazole had a low risk of dietary intake and safety threat to the population. The propiconazole treatment at the recommended concentration and above significantly increased the malondialdehyde(MDA) content, relative conductivity, and osmoregulatory substances and caused the accumulation of reactive oxygen species in P. notoginseng leaves. The propiconazole treatment at half(66 g·hm~(-2)) of the recommended dose for P. ginseng significantly increased the activities of superoxide dismutase(SOD), peroxidase(POD), and catalase(CAT) in P. notoginseng leaves. The propiconazole treatment at 132 g·hm~(-2) above inhibited the activities of glutathione reductase(GR) and glutathione S-transferase(GST), thereby reducing glutathione(GSH) content. Proconazole treatment changed the proportion of 5 main saponins in the main root of P. notoginseng. The treatment with 66 g·hm~(-2) propiconazole promoted the accumulation of saponins, while that with 132 g·hm~(-2) and above propiconazole significantly inhibited the accumulation of saponins. In summary, using propiconazole at 132 g·hm~(-2) to prevent and treat P. notoginseng diseases will cause stress on P. notoginseng, while propiconazole treatment at 66 g·hm~(-2) will not cause stress on P. notoginseng but promote the accumulation of saponins. The effect of propiconazole on P. notoginseng diseases remains to be studied.

Objective: To observe the effect of electroacupuncture(EA) on the expression of peroxisome proliferator-activated receptor gamma coactivators-1-alpha (PGC-1α), Irisin and brain-derived neurotrophic factor (BDNF) in the ischemic peripheral cortex, hippocampus and local skeletal muscle in rats with focal cerebral ischemic/reperfusion injury (CI/RI), so as to explore its underlying mechanism of improving of CI/RI., Methods: Male SD rats were randomly divided into 3 groups: sham-operation, model and EA (11 rats in each group). The focal CI/RI model was established by middle cerebral artery occlusion (MCAO). EA (2 Hz /15 Hz, 2 to 4 mA) was applied to "Quchi" (LI11) and "Zusanli" (ST36) of the affected side for 20 min, once a day for 7 days. Zea-Longa's score and Balance Beam score were used to evaluate the neurological and motor functions. The infarcted volume of the brain was detected by using 2,3,5-triphenyltetrazolium chloride staining. The expression levels of PGC-1α, fibronectin type III domain-containing protein 5(FNDC5) and BDNF proteins in the ischemic peripheral cortex, hippocampus and local skeletal muscle were detected by Western blot., Results: Compared with the sham-operation group, the Zea-Longa's score, Balance Beam score, percentage of cerebral infarct volume were notably increased ( P <0.01), while the expression levels of PGC-1α, FNDC5 and BDNF proteins in the cerebral cortex and hippocampus (not in the local muscle) were significantly down-regulated in the model group ( P <0.01, P <0.05). In comparison with the model group, the increase of Zea-Longa's score, Balance Beam score, percentage of cerebral infarct volume, and the decrease of expression levels of PGC-1α, FNDC5 and BDNF proteins in the ischemic peripheral cortex and that of BDNF in the hippocampus were reversed in the EA group ( P <0.01, P <0.05). No significant changes were found in the expression levels of hippocampal PGC-1α and FNDC5 proteins in the hippocampus and those of PGC-1α, FNDC5 and BDNF proteins in the local muscle after EA intervention ( P >0.05)., Conclusion: EA can improve neurological and motor functions and reduce cerebral infarction volume in CI/RI rats, which may be related to its functions in activating PGC-1α/Irisin(FNDC5)/BDNF pathway in the cerebral cortex.

Ischemic stroke is a major cause of permanent disability and death in adults, and electroacupuncture (EA) intervention has a positive role in improving neurological function in patients with ischemic stroke through a series of complex processes. In the present paper, we make a review about the development of researches on the involvement of micro-ribonucleic acid (miRNA) in ischemic stroke from excitatory amino acid toxicity, oxidative stress, inflammatory response, apoptosis and necrosis, and particularly sum up outcomes of researches about the roles of miRNAs in EA-induced improvement of neurological function in experimental cerebral ischemia animals. EA treatment can 1) balance levels of miRNAs (such as mir-126 and mir-328, etc.) to promote angiogenesis of ischemic cerebral cortex tissue by regulating expression of vascular endothelial growth factor family genes and proteins; 2) promote nerve regeneration by up-regulating serum miR-124 and hippocampal miR-132 expression to possibly facilitate cerebral repair and reduce cognitive dysfunction respectively via related proteins; 3) reduce cerebral edema via modulating expression of some miRNAs to control expression of aquaporin, matrix metalloproteinases, etc. and 4) suppress inflammatory response via up-regulating expression of miRNAs to inhibit expression of NF-κB, TNF-α, etc. in the local cerebral tissue. As a result, the neurological function is bettered after EA intervention.

Objective: To compare therapeutic effects between the normal rehabilitation and combined with manipulative method after arthroscopic capsular release for the treatment of severe frozen shoulder, and to evaluate the application value of manipulationp., Methods: From March 2007 to July 2010,arthroscopic capsular release was performed in 48 cases (48 shoulders, 23 left side, 25 right side). All the patients were divided into two groups: control group (11 males and 15 females) and manipulation group (9 males and 13 females). The patients in the control group were treated with conventional rehabilitation procedure, and the patients in the manipulation group were treated with additional manipulation procedure. From the 2nd day after operation, the manipulation was performed for 20 minutes every time, twice daily, and it continued for 10 days. All the cases were followed up and the scale of American Shoulder and Elbow Surgeons Standardized Assessment Form (ASES self-report section) and the range of motion (ROM) were recorded., Results: The mean follow-up period was (12.54 +/- 5.78) months (ranging from 4 to 25 months). Both ASES scores and ROM in the manipulation group were better than those in the control group at the 1st month after operation, and the difference between the ASES scores and flexion of the shoulder were significant. However, there was no significan difference at the latest follow-up., Conclusion: Compared with the conventional rehabilitative procedure, manipulation following arthroscopic capsular release could promote the process of joint rehabilitation and help the patient back to normal life earlier, but there is no evidence of long term advantage.

Background: Total knee replacement surgery is commonly used in end-stage diseases of the knee. It is important for improving surgical efficacy and patient satisfaction by promoting early rehabilitation of patients and improving knee function., Objective: To observe the effects of early application of Tuina treatment on quadriceps surface electromyography (EMG) in patients with rheumatoid arthritis having undergone total knee arthroplasty., Design, Setting, Participants and Intervention: The study was performed at the Orthopedic Department of Huashan Hospital, Fudan University, and the Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine from June 2010 to September 2011. A total of 66 patients with rheumatoid arthritis who had undergone total knee replacement surgery were randomly divided into control group and observation group, 33 cases in each. The patients in the control group were administered with continuous passive training (CPM), and the patients in the observation group were treated with CPM combined with Tuina, from prior surgery to four weeks post-surgery., Main Outcome Measures: The knee function was evaluated using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) questionnaire at baseline and 4 weeks after the surgery. Quadriceps surface EMG was also detected at the same time points., Results: After 4 weeks of Tuina and comprehensive rehabilitation intervention, the WOMAC questionnaire score of the observation group was decreased compared with the control group (P<0.01); median frequency and integrated electromyography of the rectus femoris and vastus medialis muscles, which were recorded by EMG, in the observation group were higher than those in the control group (P<0.01)., Conclusion: Tuina can improve the recovery of patients who have undergone total knee replacement by increasing quadriceps EMG.

To study whether recombinant human erythropoietin (rhEPO) reduces neuronal apoptosis through inhibiting over-expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in nucleus induced by brain ischemia/reperfusion in rats, 48 adult Sprague-Dawley rats were randomly divided into 3 groups: sham, saline and EPO groups. Animal models of brain ischemia/reperfusion were established by middle cerebral artery occlusion in rats. The effects of EPO on the sizes of ischemia tissue were observed by TTC staining. The over-expression of GAPDH in nucleus was detected by Hoechst-33258 and anti-GAPDH antibody double staining. The neuronal apoptosis in penumbral was detected by Nissl's staining and Hoechst-33258 immunofluorescence, respectively. The results showed that rhEPO treatment (3 000 U/kg, three times daily, i.p.) apparently reduced the sizes of infarct brain tissue in ischemia/reperfusion rats. rhEPO inhibited over-expression of GAPDH in nucleus of apoptotic neurons. In the meantime rhEPO decreased the number of apoptotic neurons in ischemia/reperfusion rats. These results suggest that rhEPO may induced reduction of neuronal apoptosis in penumbra may be through inhibiting over-expression of GAPDH in nucleus of apoptotic neurons induced by ischemia/reperfusion. Reduction of GAPDH over-expression in nucleus may play a pivotal role in EPO inhibiting neuronal apoptosis in cerebral ischemia/reperfusion rats, providing experimental evidence for EPO neuro-protecting effects against ischemia/reperfusion.

Objective: To observe the effects of puerarin on ADRP gene mRNA expression in fatty tissue of type 2 diabetes mellitus rats (T2DM)., Method: Wiastar rats of T2DM model were made by feeding with high glucose and fat diet and injecting with small dose of streptozocin (25 mg x kg(-1)). 40 model rats were randomly divided into model control group and three puerarin groups (40, 80, 160 mg x kg(-1)), another 10 rats were selected as normal control group. FBG and FINS were measured to calculate IR after rats were injected consecutively for 6 weeks. The level of ADRP gene mRNA in fatty tissue was determined by RT-PCR after rats were injected eight weeks., Result: Compared with model control group, high and middle dosage of puerarin can decreased ADRP gene mRNA expression in fatty tissue obviously, FBG, IR level in each puerarin group and FINS in high and middle dosage puerarin groups decreased obviously., Conclusion: Puerarin can decrease the blood glucose level of T2DM by downregulating ADRP mRNA expression and depressing the insulin resistance.

Objective: To explore the exact role of ghrelin in glyco- and lipo-metabolism., Methods: We compared the levels of ghrelin mRNA in gastric tissue, ghrelin in gastric tissue and plasma among LETO rats( non diabetes, n=10), OLETF rats( type 2 diabetes, n=10), OLETF/M rats( OLETF rats managed with Metformin at the dose of 100 mg/kg weight, n=10) and OLETF/F rats( OLETF rats managed with Fenofibrate at the dose of 20 mg/kg weight, n=10). The levels of ghrelin mRNA were tested by Northern blotting, and the ghrelin content in gastric tissue and plasma detected by RIA., Results: At the age of 30 weeks, the ghrelin fasting plasma levels of OLETF rats were lower than those of LETO rats(37.49+/-6.42 vs 58.52+/-5.85, P<0.05). The fasting blood plasma ghrelin levels of OLETF/M groups showed an increased tendency, but the difference of the fasting blood plasma ghrelin levels to those of the untreated OLETF rats were not noticeable(49.65+/-6.76 vs 37.49+/-6.42,P>0.05). However, the fasting blood plasma ghrelin levels of OLETF/F group were more than those that of the untreated OLETF rats (62.02+/-7.35 vs 37.49+/- 6.42,P<0.05). The mRNA and polypeptide levels of ghrelin in stomach tissue had no marked difference in the 4 groups at the age of 17 weeks. At the age of 30 weeks, the difference of mRNA(1.18+/-0.06 vs 1.27+/-0.05,P<0.05) and polypeptide (114.77+/- 31.65 vs 152.87+/-18.24, P<0.05) between OLETF group and LETO group had been observed. Metformin didn't influence the mRNA and polypeptide levels of ghrelin in stomach tissue markedly. Howere, the polypeptide (161.75+/-23.61 vs 114.77+/-31.65, P<0.05) and mRNA(1.36+/-0.09 vs 1.18+/-0.06,P<0.05) levels of ghrelin in stomach tissue of OLETF/F group were markedly higher than those of stomach tissue ghrelin in the untreated OLETF group., Conclusion: Our data demonstrate that ghrelin may play a role in protective, compensative and negative-feedback regulation in the disorder of glucose and lipid metabolism.

Objective: To explore the possible molecular mechanism of abnormal renal lipid metabolism in OLETF rats, and the effects of fenofibrate or metformin on renal local lipid metabolism., Methods: OLETF rats were randomly divided into three groups: one treated with fenofibrate, one with metformin and one without treatment. LETO rats were used as age-matched normal controls. The animals were sacrificed and the kidneys were obtained respectively at the age of 17 and 30 weeks. 24-hour urine albumin contents and TG contents in renal cortex were measured.The levels of SREBP-1 protein and mRNA in kidney were measured. FAS mRNA and ACC mRNA expressions were measured with RT-PCR., Results: OLETF rats showed characters of obesity, hyperglycemia, hyperlipidemia. At the end of thirty weeks clinical characters of renal damage appeared in OLETF rats, OLETF rats showed higher levels of 24-hour urine albumin contents than those of LETO rats. 24-hour urine albumin contents were correlated positively with TG contents in kidney. The partial correlation coefficient was 0.870 (P = 0.011) by controlling for body weight, serum lipid, blood glucose and fasting insulin concentration. OLETF rats showed higher levels of SREBP-1 protein (43.2%, P<0.01), FAS mRNA (126.0%, P<0.01), ACC mRNA (72.3%, P<0.01) than those of group LETO. OLETF/F rats showed lower levels of SREBP-1 (15.7%, P = 0.061), FAS mRNA (36.8%, P<0.05), ACC mRNA (40.3%, P<0.05) than those of group OLETF. OLETF/M rats showed lower levels of SREBP-1 (19.3%, P<0.01), FAS mRNA (57.3%, P<0.01), ACC mRNA (22.5%, P<0.05) than those of group OLETF. There was no difference in SREBP-1 mRNA levels for each group., Conclusion: Renal damage occurred in OLETF rats at the prediabetes stage. 24-hour urine albumin contents were correlated positively with TG contents in kidney. SREBP-1 might aggravate fat deposition in kidney through some enzyme associated with fat synthesis, which was a possible pathogenesis of diabetic nephropathy. Treatment with fenofibrate or metformin ameliorated renal damage in OLETF rats through SREBP-1 and some enzyme regulated by it reduced fat deposit in kidney directly.

Objective: To study the plasma concentration of peptide YY3 - 36 (PYY3-36) and the expression levels of PYY mRNA of ileum and colon in dietary induced obesity (DIO) and dietary induced obesity resistant (DIO-R) rats and the relation between PYY3-36 and DIO-R rats., Methods: Thirty-six female SD rats were randomly divided into high-fat diet group (n = 27) and chow fed control group (n = 9), after 13 weeks of either a high-fat diet or chew fed diet, the high-fat diet group was subdivided into DIO and DIO-R group according to the final body weight. Weight gain, caloric intake, the concentration of PYY3-36 and the expression levels of PYY mRNA were measured and compared., Results: The total caloric intake of DIO-R rats was lower than DIO rats (P < 0.01), while no significant difference was found between DIO-R and control rats (P > 0.05). The concentration of PYY3-36 and the expressions of PYY mRNA of ileum and colon in DIO-R rats were higher significantly than that of the DIO and control rats (P < 0.01), while no significant difference was found between DIO and control group (P > 0.05), except that PYY mRNA of ileum was advanced in DIO group (P < 0.01)., Conclusion: On the High-fat diet, SD rats showed different susceptibility to obese and energy intake, increased levels of PYY3-36 and PYY mRNA might be related to dietary induced obesity resistant.

Objective: To explore the expression of uncoupling proteins (UCP) and peroxisome proliferator activated receptorgamma2 (PPARgamma2) mRNA in white adipose of high-fat diet induced obesity resistant rats., Methods: Thirty-six female SD rats were randomly divided into high-fat diet group (n = 27) and chow fed control group (n = 9), and given either high-fat diet or chow for thirteen weeks. Then the high-fat diet group was subdivided into Dietary Induced Obesity (DIO) and Dietary Induced Obesity Resistant (DIO-R) group according to the final body weight. Basic parameters, fasting blood glucose (FBG), blood lipid levels were measured and compared. Reverse transcription-polymerase chain reaction (RT-PCR) was used to measure the expression of UCP2, UCP3, and PPARgamma2 mRNA in white adipose., Results: Adipose deposits, body fat percent, TC, and TG conceration of both DIO-R and DIO groups were significantly higher than those in control group, while body weight, body fat percent and TG level were significantly lower in DIO-R than DIO rats. The expression of UCP2 and UCP3 mRNA in white adipose of DIO-R rats were significantly higher than those of DIO and control group. The expression of PPARgamma2 mRNA in white adipose of DIO-R group was significantly lower than that in DIO group., Conclusion: High-fat diet induced obesity resistance were closely associated with the increased UCP2, UCP3, and decreased PPARgamma2 mRNA in white adipose.

Objective: To investigate the relationship between fasting serum levels of leptin, glucose, insulin resistance, lipids in simple obese children., Methods: Fasting serum levels of leptin and insulin (Fins) were measured by RIA in 42 obese and 42 normally-weighted children matched on age, sex and height, and their total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) were analyzed with enzymatic methods. HOMA-IR and LDL-C were calculated., Results: Serum level of leptin was (2.74 - 45.12) micro g/L and (0.53 - 10.18) micro g/L in obese and normally-weighted children, respectively, with an average level of leptin (log) significantly higher in obese group than that in control group (P < 0.001). Serum level of leptin was positively correlated with BMI, WHR and percentage of body fat. Of obese children, 83% were leptin resistant. Serum levels of TC, TG, LDL-C and insulin were significantly higher in obese leptin-resistant group than those in normally-weighted control group, but no significant difference in them between obese leptin-sensitive group and its normally-weighted control group was observed. Significantly higher serum levels of TG and lower HDL-C were observed in obese leptin-resistant group, as compared with those in obese leptin-sensitive group., Conclusions: A big difference in serum level of leptin between obese and normally-weighted children was found, suggesting most obese children were resistant to endogenous leptin. Leptin resistance correlated significantly with the risk of metabolic syndrome and cardiovascular disease, indicating serum level of leptin could be used as an indicator in screening obese children at high risk.