Journal of Traditional Chinese Medicine最新文献

Protein losing enteropathy (PLE), a very rare disease with hypoproteinemia and edema as its characteristics, is caused by various diseases resulting in protein depletion from the gut. The diagnosis is relatively difficult due to its complex pathogeneses. The present paper reported a case whose symptom started with acute diarrhea and hypoproteinemia. Gastrointestinal endoscopies showed digestive ulcers and colon polyp. The treatments contained albumin infusion, Chinese herbal decoction and other symptomatic therapies. The hypoproteinemia become even worse and edema occurred after 4 days' treatment. A larger dose of albumin infusion (40-60 g/d) and modified herbal decoctions were prescribed. A final diagnosis of eosinophilic gastroenteritis (EG) complicated with PLE was confirmed by histopathological examination of a repeated gastroscopy. After three weeks' treatment, the serum albumin level was raised and the edema subsided gradually. In conclusion, herbs may have an effect on PLE patients, but PLE resulting from EG is very complex and easy to misdiagnose, especially in atypical conditions. Further studies are required to find the exact mechanisms.

OBJECTIVE

To investigate effect of Yupingfeng granules, prepared with Chinese Medicines, on the wound healing and on the expression of aquaporin 3 (AQP3) and the skin barrier in the animal models of atopic dermatitis (AD).

METHODS

Acute skin lesions of AD models were prepared using 2,4-dinitrochlorobenzo (DNCB) in mice and animals were treated with either Yupingfeng granules or placebo for two weeks. Skin wound healing outcome was assessed by measuring skin thickness, weight (quality) of the skin, and trans-epidermal water loss (TEWL). Expression of AQP3 mRNA and protein was assessed by reverse transcriotion polymerase chain reaction (RT-PCR) and immunoblotting, respectively.

RESULTS

Yupingfeng granule treatment resulted in significant acceleration of wound healing with 63.64% efficiency, which was significantly higher than that of placebo granule treatment (31.82%, P < 0.01 by Wilcoxon Rank-sum test). Skin thickness, weight of the wounded skin, and TEWL were significantly higher in the AD models compared to that of normal animals. Treatment with Yupingfeng granules resulted in significant decrease in skin thickness [(937 ±31) vs (360 ±21) urn, P < 0.01], weight of the wounded skin [(42 ± 4) vs (24 ± 5) mg, P < 0.01], and TEWL [(30 ±4) vs (13 ± 4) g • h⁻¹ • m⁻², P < 0.01]. Yupingfeng granules also significantly down-regulated mRNA and protein expression of AQP3 in the animal models.

CONCLUSION

Our findings suggested that Yupingfeng granules could be used in AD treatment.

OBJECTIVE

To investigate the effects of Shenqi Yangxin decoction (SQYXD) on heart function in a rat model of dilated cardiomyopathy (DCM) and its potential mechanisms.

METHODS

Sprague-Dawley rats were randomly divided into normal (10 rats) and DCM (150 rats) groups. DCM was induced by an intraperitoneal injection of adriamycin. Then, DCM baseline group was randomly selected sixteen DCM rats. The remaining DCM rats were randomly divided into DCM control, perindopril, metoprolol, and SQYXD groups. Cardiac function and histological analysis plus biochemical measurement of serum levels of brain natriuretic peptide (BNP), and inflammatory factors were measured. The mRNA and protein expression levels of high-mobility group box 1 (HMGB1), Toll-like receptor 4 (TLR-4), receptor for advanced glycation end products (RAGE), and nuclear factor-κB (NF-κB) were determined. Myocardial metabolism imaging was performed on the normal, SQYXD and DCM control groups to evaluate the effectiveness of treatments.

RESULTS

Rats in the DCM control group exhibited dilated left ventricular diameter, impaired cardiac function, disorganized sarcomere, impaired glucose metabolism, increased heart weight index, and increased levels of BNP, which were improved by treatment with SQYXD. In addition, hearts from rats in the DCM baseline group exhibited significantly higher levels of HMGB1, TLR-4, RAGE, NF-κB, tumor necrosis factor-α, interleukin-1, interleukin-6, interleukin-10, compared with the normal group. Interestingly, the mRNA level of HMGB1 in the DCM baseline group was positively correlated with that of TLR-4, RAGE, NF-κB, BNP, and LVEDD, but negatively correlated with LVEF. SQYXD inhibited the upregulation of HMGB1 expression and its downstream inflammatory factors.

CONCLUSION

Shenqi Yangxin decoction effectively reduced the dilated left ventricular diameter and improved heart function in dilated cardiomyopathy. The mechanisms underlying the action on DCM involve regulating the gene and protein expression of HMGB1 and its inflammatory signal pathways in the DCM rat model.

OBJECTIVE

To determine the effect of an esculetin formulation (at 97.4% purity) on osteoporosis, and to investigate the potential underlying molecular mechanism(s).

METHODS

Sixty specific pathogen free-grade female Wistar rats were randomly assigned to three groups: blank control (n = 12), sham (n = 12), and model (n = 36). The model group were bilaterally ovariectomized. The sham group had the tissue surrounding the ovaries removed, while the ovaries were retained. After 3 months, the model group was randomly divided into three subgroups: OVX (n = 12), positive control (n = 12), and esculetin (n = 12). The positive control group and the esculetin group were intragastrically administered diethylstilbestrol (0.046 mg • kg⁻¹ • d⁻¹) or esculetin (384 mg • kg⁻¹ • d⁻¹), respectively, once per day for 6 consecutive days; medication administration was then stopped for 1 d, before being administered for another 6 consecutive days. All rats were treated for 3 months. Samples were collected at the end of the treatment period. An Osteocore3 Digital 2D bone densitometer was used to test the bone mineral density, and histomorphometric analysis was performed to measure bone mass, bone formation, and bone resorption. Enzyme-linked immunosorbent assay analysis was used to measure the serum concentrations of interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor-kappa B ligand (RANKL). Immunohistochemistry and in situ hybridization were performed to detect the protein and mRNA expressions of OPG and RANKL in osteoblasts and bone marrow stromal cells.

RESULTS

Compared with the OVX group, the esculetin group had significantly greater femoral bone mineral density and tibial trabecular bone volume, and significantly smaller trabecular resorption surface. The percentage of trabecular formation surface, average osteoid width, trabecular bone mineralization rate, and cortical bone mineralization rate did not significantly differ between groups. Compared with the sham group, the esculetin group had significantly decreased serum levels of IL-6 and RANKL, and significant downregulation of RANKL protein and mRNA expression levels in osteoblasts and bone marrow stromal cells; however, there was no significant difference between groups in OPG.

CONCLUSION

Esculetin can increase bone mass by upregulating RANKL expression in osteoblasts and bone marrow stromal cells, and decreasing serum IL-6 concentration. This indicates that the therapeutic effect of esculetin on osteoporosis occurs via decreased bone resorption.

OBJECTIVE

To evaluate the risk of ischemic stroke endpoints by establishing risk assessment models that combine Traditional Chinese Medicine (TCM) and modern medicine indicators.

METHODS/DESIGN

The proposed study is a registry-based participant survey conducted in seven hospitals nationwide in China. After obtaining informed consent, 3000 patients diagnosed with ischemic stroke will be recruited. One-year follow-ups will be performed on-site in hospitals and by telephone to track endpoint events. Comparative analysis of the prevalence of endpoint events and other TCM or modern medicine features in different groups will be conducted using frequency analysis and χ² tests, and the results will be expressed as composition ratios. Comparative analysis of quantitative scores and related patterns or symptoms will be conducted using a rank-sum test. Correlation analysis of endpoint events and TCM or modern medicine factors will be performed using a multivariate Cox proportional hazard model.

DISCUSSION

Previous reports have described modern medicine indicator-based risk assessment models for ischemic stroke endpoint events, but no such studies have included TCM features. Our new risk assessment model combines TCM and modern medicine indicators and thus has the potential to facilitate early warning, early intervention, and early control of ischemic stroke endpoint events.

OBJECTIVE

To investigate the effect of Jianpi Bushen (JPBS) formula on aromatase inhibitor (AI)-associated bone loss after menopause.

METHODS

Six-month-old female rats were randomly divided into 6 groups: a sham group, an ovariectomized (OVX) group, an OVX treated with exemestane and 3 OVX groups each treated with a different dose of JPBS formula. Bone mineral density (BMD) at the lumbar vertebrae, histology, bone markers and serum levels of estrogen were assessed. Furthermore, a cohort study was conducted in 130 postmenopausal women with breast cancer that had undergone treatment with Als. The subjects were given JPBS + caltrate D or caltrate D only, administered orally. BMD at the lumbar vertebrae and femoral neck and bone markers were evaluated in both control and herbal treatment groups at baseline and 12 months.

RESULTS

Experimental results indicated that a high dose of JPBS significantly increased the trabecular bone area percentage (Tb.Ar %) and broadened the trabecular thickness (Tb.Th). The JPBS formula enriched the carboxyterrninal propeptide of type ipmcollagen and increased serum estrogen level significantly. The clinical investigation revealed that bone loss was decreased in the group treated with JPBS vs control (BMD T score at lumbar vertebrae, 3.9% increased vs 14.58% decreased, respectively, P = 0.004 and BMD T score on femoral neck, 1.8% decreased vs 22.45% decreased, respectively, P = 0.008). Besides, JPBS formula elevated N-middle osteocalcin and decreased type I collagen cross-linked C-terminal telopeptide.

CONCLUSION

JPBS formula prevented aromatase-inhibitor-associated bone loss after menopause by inhibiting bone resorption and promoting bone formation.

OBJECTIVE

To examine the effects of Cuzhi liquid on learning and memory abilities in a mouse model of Alzheimer's disease (AD).

METHODS

One hundred mice were divided into the normal, AD model, piracetam group, Cuzhi liquid low dose and Cuzhi liquid high dose, each group 20 mice. The AD mouse model was induced by daily intraperitoneal injection of D-galactose and sodium nitrite. AD mice then received intragastric administration of piracetam or Cuzhi liquid for 60 d, and changes in learning and memory abilities were assessed using the water maze test. The activity of acetylcholinsterase (AchE) and monamine oxidase (MAO), and the levels of nitrogen monoxidum (NO) and malonaldehyde (MDA), were measured in brain tissues. Amyloid protein deposition was assessed by methyl violet staining, and B-cell lymphoma-2 (Bcl-2) expression in the hippocampal cornus ammonis 1 region was detected by immunohistochemistry.

RESULTS

In the water maze test, the escape latency of the model group was longer than that of the normal group (P < 0.01). The escape latency of the three using drug treatment groups was significantly less than that of the normal group (P < 0.05). The activity of AchE and MAO, and the levels of NO and MDA, in the brain of the model group were significantly higher than that of the normal group (P < 0.01), but significantly reduced in the three drug treatment groups compared with the model group (P < 0.05). AchE activity showed a greater reduction in the two Cuzhi liquid groups compared with the piracetam group (P < 0.01), to levels similar to the normal group. There were no differences in MAO activity or NO levels between the three drug treatment groups, while MDA levels were reduced more in the high-dose Cuzhi liquid group compared with the other treatment groups (P < 0.01). Hippocampal Bcl-2 expression was significantly reduced in the model group compared with the normal group (P < 0.01), but significantly improved in the three drug treatment groups (P < 0.05). The high-dose Cuzhi liquid group showed a significantly greater recovery in Bcl-2 expression compared with the other treatment groups.

CONCLUSION

Cuzhi liquid can improve learning and memory impairment in an AD mouse model. The mechanism of action may relate to reduced AchE and MAO activity, and reduced NO and MDA levels, in the brain, and improved Bcl-2 expression, an inhibitor of apoptosis.

OBJECTIVE

To evaluate vitality principle in breast cancer rats by pharmacologically developing a model for anticancer surveillance.

METHODS

The breast cancer in rats was replicated with 7,12-Dimethylbenz[a]anthracene (DMBA, i.g., 100 mg/kg) at d₀₀₁. The anticancer surveillance was defined as the intervals between the primary sensitization and the first challenge stirred with complete Freund's adjuvant (CFA), the various intervals (k = 0.80) were dominated from d₀₂₅ (600.00 h) to d₀₉₅ (2288.82 h). The optimal surveillant status was confirmed with the median effective interval (EI₅₀) from tumor volume regressive curve, for developing the pharmacodynamic model. The tumor and tumor infiltrating lymphocyte histopathology was used to confirm the immune surveillance being affected with CFA in breast cancer tumorigenesis. The availability of this model was confirmed with Shugan Liangxue prescription (SLP), from the vitality principle, and assured further from interleukin-12 levels.

RESULTS

The regressive curve was set up between the intervals and tumor volumes, the EI₅₀ in SLP-treated rats (1475.00 h, Y_SLP = 0.1026 + 0.8780/[1 + 10^{(27.1425-8.565×)}]) was postponed, which was 1.87 multiple of the EI₅₀ in CFA rats (791.40 h, y = −0.0525 + 0.9452/[1 + 10^{(30.4870-10.52×)}], so did prepone the curve between the intervals and the immunological biomarker, serum inter-leukin-12 levels, the EI₅₀ in SLP-treated rats (744.90 h, Y_SLP = −0.0145 + 0.7455/[1 + 10^{(52.09636-18.13×)}]) be 0.78 multiple of the EI₅₀ in CFA rats (960.10 h, Y_CFA = 0.2460 + 0.7270/[1 + 10^{(− 67.1546 + 22.52×)}]), this immunological action being mediated the anticancer prognosis. Tumor histology was confirmed the more tumor infiltrating lymphocytes activated in SLP rats with CFA stirred immunity than rats only received CFA.

CONCLUSION

The model for anticancer surveillance was pharmacologically established as the optimal interval (791.40 h) between the primary sensitization and the first challenge stirred with complete Freund's adjuvant. This available model was confirmed with SLP, from the vitality principle, for evaluating immunological effects against breast cancer.

The pathogenic mechanism of diabetic kidney disease (DKD) is complex. The development of DKD cannot be fully explained by a single mechanism. Traditional Chinese Medicine (TCM) has been applied extensively for the treatment of DKD in China. However, studying the mechanism of DKD using theories and methods that are appropriate for TCM characteristics and searching for theoretical bases for TCM clinical application are topics that still need to be explored and researched. Activation of the transforming growth factor (TGF)-β1/Smad and PI3K/Akt/mTOR signaling pathways functions as a self-protection mechanism against renal microinflammation in DKD. However, the persistent abnormal overactivation of reactions causes secondary cell dysfunction, cell apoptosis, increased extracellular matrix (ECM) secretion, and eventually renal fibrosis. During this process, the dysregulation of self-balance among a variety of signaling pathways and the loss of self-feedback regulatory mechanisms downstream of these signaling pathways are critical causes of the occurrence and development of DKD. TCM may both inhibit the expression or activation of “hyperactive” signaling pathways (NFB, Smad3, and PI3K/Akt/mTOR) and increase the expression or activation of “deficient” signaling pathways (Smad7 and PTEN) to restore balance to cells with an abnormal pathophysiological status and achieve the goal of DKD treatment.