Efficacy and safety of Tuina and intermediate frequency electrotherapy for frozen shoulder: MRI-based observation evidence.

BACKGROUND: Tuina and Intermediate Frequency (IF) electrotherapy are commonly used treatments for frozen shoulder (FS). This study aimed to compare the clinical efficacy of Tuina and IF electrotherapy in the treatment of stage II frozen shoulder and to provide evidence-based treatment for FS. METHODS: The FS patients were randomized into two groups, the observation group, which received Tuina, and the control group, which received IF electrotherapy. The total treatment duration was 20 minutes per treatment, 3 times per week; the treatment period was 6 weeks. Assessments were performed at baseline, 3 weeks, 6 weeks, and 16 weeks after follow-up. Primary assessments included visual analog scale (VAS), Constant-Murley scale (CMS), and secondary assessments included shoulder MRI, rotator cuff muscle diffusion tensor imaging (DTI). RESULTS: A total of 57 patients participated in this study, in the observation group (n = 29) and the control group (n = 28). At the end of the 3rd and 6th weeks of treatment, Tuina was significantly more effective than IF electrotherapy in reducing the VAS score and improving the Constant-Murley total score (P<0.05), but there was no significant difference in scores between the two groups at the 16-week follow-up (P>0.05). MRI results in both groups: compared to the control group, the observation group had better results in reducing the degree of periapical edema and reducing the thickness of the axillary humeral capsule (P<0.05); and the observation group had significantly more efficacy than the control group in improving the diffusion state of water molecules in the rotator cuff muscles (P<0.05). CONCLUSION: Tuina is more effective than IF electrotherapy in improving the symptoms of FS patients as it can rapidly relieve the pain and restore the function of the affected shoulder, reduce the edema of the shoulder capsule, restore the function of the rotator cuff muscles, and shorten the natural course of FS. Name of the registry: This study was registered in the Shandong University of Traditional Chinese Medicine Affiliated Hospital; Grant No. (2021) Lun Audit No. (033) - KY; Date of registration: 2021.4.27.

Alantolactone ameliorates cancer cachexia-associated muscle atrophy mainly by inhibiting the STAT3 signaling pathway.

BACKGROUND: Cancer cachexia is a serious metabolic disorder syndrome that is responsible for the deaths of approximately 30% of patients with cancer, but effective drugs for cancer cachexia are still lacking. Inflammatory cytokines such as TNF-α or IL-6 are involved in the induction of skeletal muscle atrophy and fat depletion in patients with cancer cachexia. PURPOSE: In this study, we assessed the therapeutic effects of the natural compound alantolactone (AL) on cancer cachexia and tried to clarify the mechanisms by which it ameliorates muscle atrophy. METHODS: The C26 tumor-bearing cancer cachexia mouse model was used to evaluate the efficacy of AL in alleviating cancer cachexia in vivo. The levels of IL-6 or TNF-α in mouse serum were detected using ELISA kits. Cultured C2C12 myotubes and 3T3-L1 adipocytes treated with conditioned medium of C26 tumor cells, IL-6 or TNF-α were employed as in vitro cancer cachexia models to examine the effects of AL in vitro. RESULTS: AL (5 or 10 mg/kg, qd, i.p.) protected mice with C26 tumors and cachexia from a loss of body weight and muscle wasting but only slightly ameliorated fat loss. The circulating level of IL-6 but not TNF-α was significantly decreased by AL. AL treatment significantly inhibited STAT3 activation in the gastrocnemius (GAS) muscle of cancer cachexia mice. AL (0.125, 0.25, 0.5 and 1 µM) dose-dependently ameliorated myotube atrophy and STAT3 activation in cultured C2C12 myotubes induced by conditioned medium from C26 tumor cells. AL also ameliorated C2C12 myotube atrophy induced by IL-6 and inhibited IL-6-mediated STAT3 activation. AL exhibited weak effects on ameliorating TNF-α-mediated myotube atrophy and NF-κB activation. Only AL at high doses of more than 5 µM ameliorated lipolysis and STAT3 activation induced in mature 3T3-L1 adipocytes by conditioned medium from C26 tumor cells. CONCLUSIONS: AL significantly ameliorated muscle atrophy in a cancer cachexia model mainly through the inhibition of the STAT3 pathway. AL might be a promising lead compound in the development of drug candidates for cancer cachexia therapy.

Establishment of a mouse model of cancer cachexia with spleen deficiency syndrome and the effects of atractylenolide I.

Cancer cachexia is a multifactorial metabolic syndrome that affects ∼50%-80% of cancer patients, and no effective therapy for cancer cachexia is presently available. In traditional Chinese medicine, a large portion of patients with cancer cachexia was diagnosed as spleen deficiency syndrome and treated with tonifying TCMs that produce clinic benefits. In this study we established a new animal model of spleen deficiency and cancer cachexia in mice and evaluated the therapeutic effects of atractylenolide I, an active component of tonifying TCM BaiZhu, in the mouse model. Cancer cachexia was induced in male BALB/c mice by inoculation of mouse C26 colon adenocarcinoma cells, whereas spleen deficiency syndrome was induced by treating the mice with spleen deficiency-inducing factors, including limited feeding, fatigue, and purging. The mouse model was characterized by both cachexia and spleen deficiency characteristics, including significant body weight loss, cancer growth, muscle atrophy, fat lipolysis, spleen, and thymus atrophy as compared with healthy control mice, cancer cachexia mice, and spleen deficiency mice. Oral administration of atractylenolide I (20 mg· kg-1per day, for 30 days) significantly ameliorated the reduction in body weight and atrophy of muscle, fat, spleen, and thymus in mice with spleen deficiency and cachexia. The established model of spleen deficiency and cancer cachexia might be useful in the future for screening possible anticachexia TCMs and clarifying their mechanisms.

Analysis of dencichine by HPLC with pre-column derivatization / 中国中药杂志

<p><b>OBJECTIVE</b>To establish a reversed-phase high performance liquid chromatorgraphy (RP-HPLC) method for detecting the dencichine in Panax notoginseng extracts and drug preparations.</p><p><b>METHOD</b>Dencichine was extracted with the borate buffer (pH 9. 18) and the clear supernatant was used for the derivatization. Pre-column derivatization was performed using 9-fluorenylmethyl chloroformate (FMOC) to form derivatives. The mobile phase consisted of methanol and 0. 05 mol x L( -1) NaH2 PO4 (48: 52) (pH adjusted to 7.4 with NaOH solution) in a flow rate of 1.0 mL m min(-1). The ultraviolet (UV) detection wavelength was set at 262 nm.</p><p><b>RESULT</b>The linearity was demonstrated over a wide range of concentration from 1.76 mg L(-1) to 352 mg x L(-1) for dencichine. The detection limit was determined to be 60 microg x L(-1). The derivative was stable and the derivatization agent did not influence the measurement of dencichine. The average recovery rate was 95. 3% and the relative standard derivation (RSD) was 1. 7%. The method was used to determine dencichine in different P. notoginseng extracts and drug preparations.</p><p><b>CONCLUSION</b>This method is simple, fast and sensitive, suitable for determining the dencichine in P. notoginseng extracts and drug preparations as well as for the study of the dencichine metabolism in vivo.</p>