The effectiveness of balneotherapy and aquatic exercise on bone metabolism: A systematic review and meta-analysis.

OBJECTIVE: To systematically evaluate the effectiveness of balneotherapy and/or aquatic exercise on bone metabolism. DESIGN: A systematic literature search was conducted from inception to January 4, 2021. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated using a fixed-effect model according to study heterogeneity. RESULTS: Seven articles involving 467 participants were selected. Three balneotherapy studies were qualitatively integrated. The results showed that bone resorption slowed down with or without stimulation of bone formation. A pooled meta-analysis of four studies on aquatic exercise showed significant evidence for a reduction in parathyroid hormone (PTH; SMD = -0.71; 95% CI, -1.04 to -0.38; P < 0.001), and a significant increase in osteocalcin (OC; SMD = 0.60; 95% CI, 0.16 to 1.03; P = 0.007) after aquatic exercise. CONCLUSION: Balneotherapy and aquatic exercise had significant effects on bone metabolism, reducing bone resorption and/or increasing bone formation. This study highlights the importance of balneotherapy and aquatic exercise for bone health.

Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway.

Calorie restriction (CR) is a nongenetic intervention with a robust effect on delaying aging in mammals and other organisms. A mild stimulation on mitochondrial biogenesis induced by CR seems to be an important action mode for its benefits. Here, we reported that a component isolated from Rhodiola rosea L., salidroside, delays replicative senescence in human fibroblasts, which is related to its stimulation on mitochondrial biogenesis by activating SIRT1 partly resulted from inhibition on miR-22. Salidroside increased the mitochondrial mass that accompanied an increment of the key regulators of mitochondrial biogenesis including PGC-1α, NRF-1, and TFAM and reversed the mitochondrial dysfunction in presenescent 50PD cells, showing a comparable effect to that of resveratrol. SIRT1 is involved in the inducement of mitochondrial biogenesis by salidroside. The declined expression of SIRT1 in 50PD cells compared with the young 30PD cells was prevented upon salidroside treatment. In addition, pretreatment of EX-527, a selective SIRT1 inhibitor, could block the increased mitochondrial mass and decreased ROS production induced by salidroside in 50PD cells, resulting in an accelerated cellular senescence. We further found that salidroside reversed the elevated miR-22 expression in presenescent cells according to a miRNA array analysis and a subsequent qPCR validation. Enforced miR-22 expression by using a Pre-miR-22 lentiviral construct induced the young fibroblasts (30PD) into a senescence state, accompanied with increased senescence-related molecules including p53, p21, p16, and decreased SIRT1 expression, a known target of miR-22. However, salidroside could partly impede the senescence progression induced by lenti-Pre-miR-22. Taken together, our data suggest that salidroside delays replicative senescence by stimulating mitochondrial biogenesis partly through a miR22/SIRT1 pathway, which enriches our current knowledge of a salidroside-mediated postpone senility effect and provides a new perspective on the antidecrepitude function of this naturally occurring compound in animals and humans.

Salidroside protects SH­SY5Y from pathogenic α­synuclein by promoting cell autophagy via mediation of mTOR/p70S6K signaling.

The abnormal aggregation of α­synuclein (α­syn), which is an important pathological feature of Parkinson's disease (PD), is cytotoxic to dopaminergic neurons and causes cellular damage and apoptosis. Salidroside (SAL) is the main active component of the traditional Chinese medicine Rhodiola rosea. Previous research has demonstrated that SAL exerts cellular protection against cell senescence and neurodegeneration. However, the role and mechanism of action of SAL in PD remain unclear. The present study used overexpression of the wild­type and the A53T mutation of α­syn to induce a neuronal model of PD in SH­SY5Y cells, which led to neuronal toxicity and a reduced cell proliferation index. SAL increased the cell proliferation index of both PD model groups in a dose­dependent manner. Additionally, SAL alleviated pathogenic phosphorylated (Ser129) α­syn expression as well as the ratio of microtubule­associated proteins 1A/1B light chain 3 (LC3)­I to LC3­II expression, which is related to autophagic function. Furthermore, the results suggested that the underlying mechanism for the SAL­induced protection of PD model neurons may involve the preservation of autophagy, which attenuates the phosphorylation of α­syn in neurons predominantly via mTOR/p70S6K, and is independent of the PI3K/Akt signaling pathway.

The Salutary Influence of Forest Bathing on Elderly Patients with Chronic Heart Failure.

The aim of the current study was to test the hypothesis that forest bathing would be beneficial for elderly patients with chronic heart failure (CHF) as an adjunctive therapy. Two groups of participants with CHF were simultaneously sent to the forest or an urban control area for a four-day trip, respectively. Subjects exposed to the forest site showed a significant reduction of brain natriuretic peptide (BNP) in comparison to that of the city group and their own baseline levels. The values for the cardiovascular disease related pathological factors, including endothelin-1 (ET-1), and constituents of the renin-angiotensin system (RAS), including renin, angiotensinogen (AGT), angiotensin II (ANGII), and ANGII receptor type 1 or 2 (AT1 or AT2) in subjects exposed to the forest environment were lower than those in the urban control group. Obviously, a decreased level of inflammatory cytokines and improved antioxidant function was observed in the forest group rather than in the city group. The assessment of the profile of mood states (POMS) indicated that the negative emotional mood state was alleviated after forest bathing. As anticipated, a better air quality in the forest site was observed according to the detection of PM2.5 (particulate matter <2.5 µm) and negative ions. These results provided direct evidence that forest bathing has a beneficial effect on CHF patients, and thus may pave the way for potential development of forest bathing as an effective adjunctive therapy on cardiovascular disorders.

Preventive Effects of a Natural Anti-Inflammatory Agent, Astragaloside IV, on Ischemic Acute Kidney Injury in Rats.

This study investigated the anti-inflammatory effects of astragaloside IV(AS-IV) on ischemia/reperfusion (IR) induced acute kidney injury (AKI) in rats. Experimental model of ischemic AKI was induced in rats by bilateral renal artery clamp for 45 min followed by reperfusion of 12 h and 24 h, respectively. AS-IV was orally administered once a day to rats at 10 and 20 mg·kg(-1)·d(-1) for 7 days prior to ischemia. AS-IV pretreatment significantly decreased serum urea, creatinine, and cystatin C levels at 12 h and 24 h of reperfusion in AKI rats. AS-IV pretreatment also ameliorated tubular damage and suppressed the phosphorylation of p65 subunit of NF- κ B in AKI rats. Moreover, NF- κ B and MPO activity as well as serum and tissue levels of TNF- α , MCP-1, and ICAM-1 were elevated in AKI rats. All of these abnormalities were prevented by AS-IV. Furthermore, AS-IV downregulated the mRNA expression of NF- κ B, TNF- α , MCP-1, and ICAM-1 in AKI rats. These results suggest that AS-IV might be developed as a novel therapeutic approach to prevent ischemic AKI through inhibition of NF- κ B mediated inflammatory genes expression.

Antiaging effect of pine pollen in human diploid fibroblasts and in a mouse model induced by D-galactose.

The present paper was designed to investigate the effect of pine pollen against aging in human diploid fibroblast 2BS cells and in an accelerated aging model, which was established by subcutaneous injections with D-galactose daily for 8 weeks in C57BL/6J mice. Pine pollen (1 mg/mL and 2 mg/mL) is proved to delay the replicative senescence of 2BS cells as evidenced by enhanced cell proliferation, decreased SA-ß-Gal activity, and reversed expression of senescence-associated molecular markers, such as p53, p21(Waf1), p16(INK4a), PTEN, and p27(Kip1) in late PD cells. Besides, pine pollen reversed D-galactose-induced aging effects in neural activity and inflammatory cytokine levels, as indicated by improved memory latency time and reduced error rate in step-down test and decreased concentrations of IL-6 and TNF-α in model mice. Similar to the role of AGEs (advanced glycation endproducts) formation inhibitor aminoguanidine (AG), pine pollen inhibited D-galactose-induced increment of AGEs levels thus reversed the aging phenotypes in model mice. Furthermore, the declined antioxidant activity was obviously reversed upon pine pollen treatment, which may account for its inhibitory effect on nonenzymatic glycation (NEG) in vivo. Our finding presents pine pollen as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.

[Clinical observation on catgut implantation at acupoint for treatment of somatic form disorders].

OBJECTIVE: To compare therapeutic effects of catgut implantation at acupoint plus small dose of Paroxetine Hydrochloride and simple Paroxetine Hydrochloride. METHODS: Eighty-eight cases of such disease were divided into 2 groups, a treatment group (n=54) and a control group (n=34). The treatment group were treated with catgut implantation at main points Dazhui (GV 14), Zhongwan (CV 12), Tianshu (ST 25), Ganshu (BL 18), Pishu (BL 20), Shenshu (BL 23), etc., plus oral administration of small dose of Paroxetine Hydrochloride; and the control group were treated with simple Paroxetine Hydrochloride. They were treated for 6 weeks. Hamilton Depression Rating Scale (HAMD) was used for assessment of the therapeutic effect. RESULTS: The effective rate was 92.6% in the treatment group and 85.3% in the control group with a significant difference between the two groups (P < 0.05); at the end of the first week and the second week of treatment, the score for HAMD in the treatment group significantly decreased as compared with that in the control group (P < 0.01). CONCLUSION: Catgut implantation at acupoint plus small dose of Paroxetine Hydrochloride has a better therapeutic effect on somatic form disorders.