RESUMO
Objectives: This study aimed to evaluate the effectiveness and safety of proprioceptive neuromuscular facilitation for chronic low back pain.Materials and methods: Eleven databases were searched from their inception through January 2021. The primary outcomes were pain intensity, individual activities, quality of life, and adverse events. Results: Four randomized controlled trials (RCTs) with 184 patients (mean age: 37.8±3.1 years; range, 35 to 50 years) met the inclusion criteria. The pooled effect size showed proprioceptive neuromuscular facilitation, relieved pain (standard means difference [SMD]: -0.835, 95% CI: -1.139 to -0.531, p<0.001, n=4), and improved individual activity (Roland Morris Disability Questionnaire, SMD: -1.765, 95% CI: -2.642 to -0.888, p<0.001, n=2; Oswestry Disability Index, SMD: -0.893, 95% CI: -1.434 to -0.352, p=0.001, n=1) for chronic low back pain (CLBP). Conclusion: This study verified that proprioceptive neuromuscular facilitation could relieve pain and improve individual activities without serious adverse events in patients with CLBP; however, it should be cautiously recommended due to the small number of included RCTs.
RESUMO
RATIONALE: Evidences indicate that methylglyoxal, a highly reactive metabolite of hyperglycemia, can enhance protein glycation, oxidative stress, or inflammation. Mangiferin, a polyphenol compound of C-glucoside, has many beneficial biological activities, including anti-inflammation, anti-oxidation, neuroprotection, cognitive enhancement, etc. Whether mangiferin alleviates diabetes-associated cognitive impairment is still unclear. OBJECTIVES: The present study was designed to investigate the effects of mangiferin on the behavioral deficits of diabetic rats induced by streptozotocin; the mechanisms associated with methylglyoxal toxicity are especially investigated. METHODS: Diabetic rats were treated with mangiferin (15, 30, and 60 mg/kg, p.o.) for 9 weeks. Cognitive performances were evaluated with the Morris water maze. Hippocampus and blood were obtained for evaluation of the effects of mangiferin on protein glycation, oxidative stress, and inflammation in diabetic state. RESULTS: Mangiferin significantly improved the behavioral performances of diabetic rats, evidenced by a decrease in escape latency as well as increases in numbers of crossing the platform and percentage of time spent in the target quadrant, which were accompanied by decreases in the levels of advanced glycation end-products and their receptor (RAGE), interleukin-1ß, TNF-α, and malondialdehyde and increases in the activity and expression of glyoxalase 1 as well as glutathione level in the hippocampus of diabetic rats. Furthermore, mangiferin produced a significant decrease in malondialdehyde level and increased glutathione level and superoxide dismutase activity in the serum of diabetic rats. CONCLUSIONS: This study demonstrates that mangiferin can markedly ameliorate diabetes-associated cognitive decline in rats, which is done likely through suppressing methylglyoxal hyperactivity (promoting protein glycation, oxidative stress, and inflammation) mediated noxious effects.