[Role of NLRP3 inflammasome in diabetic neuropathy and prevention and treatment with traditional Chinese medicine].

As one of the most frequent complications of diabetes, diabetic neuropathy often involves peripheral and central nervous systems. Neuroinflammation is the key pathogenic factor of secondary nerve injury in diabetes. NOD-like receptor pyrin domain-containing 3(NLRP3) inflammasome is a group of subcellular multiprotein complexes, including NLRP3, apoptosis associated speck-like protein(ASC), and pro-cysteinyl aspartate specific proteinase 1(pro-caspase-1). NLRP3 inflammasome is an inducer of innate immune responses. Its activation stimulates the inflammatory cascade reaction, promotes the release of inflammatory mediators, triggers cell death and uncontrolled autophagy, activates glial cells, facilitates peripheral immune cell infiltration, and initiates amyoid ß(Aß)-tau cascade reactions. As a result, it contributes to the central nerve, somatic nerve, autonomic nerve, and retinal nerve cell damage secondary to diabetes. Therefore, due to its key role in the neuroinflammation responses of the body, NLRP3 inflammasome may provide new targets for the treatment of diabetic neuropathy. With multi-target and low-toxicity advantages, traditional Chinese medicine plays a vital role in the treatment of diabetic neuropathy. Accumulating evidence has shown that traditional Chinese medicine exerts curative effects on diabetic neuropathy possibly through regulating NLRP3 inflammasome. Although the role of NLRP3 inflammasome in diabetes and related complications has been investigated in the literature, systematical studies on drugs and mechanism analysis for secondary neuropathy are still lacking. In this article, the role of NLRP3 inflammasome in diabetic neuropathy was explored, and the research progress on traditional Chinese medicine in the treatment of diabetic neuropathy through NLRP3 inflammasome was reviewed.

Potential effect of tropical fruits Phyllanthus emblica L. for the prevention and management of type 2 diabetic complications: a systematic review of recent advances.

Phyllanthus emblica is a fruit widely consumed in subtropical areas, which is rich in polyphenols and other nutrients. There are increasing evidences that as a daily and nutritious fruit, it may have a positive role in controlling diabetic complications. According to the new study, its mechanisms include enhancing the functioning of insulin, reducing insulin resistance, activating the insulin-signaling pathway, protecting ß-cells, scavenging free radicals, alleviating inflammatory reactions, and reducing the accumulation of advanced glycation end products. Owing to its few side effects, and low price, it should be easily accepted by patients and has potential for preventing diabetes. Taken together, Phyllanthus emblica may be an ideal fruit for controlling diabetic complications. This review highlights the latest findings of the role of Phyllanthus emblica in anti-diabetes and its complications, especially clarifies the molecular mechanism of the chemical components related to this effect, and prospects some existing problems and future research directions.

Rapid, microwave-accelerated synthesis and anti-osteoporosis activities evaluation of Morusin scaffolds and Morusignin L scaffolds.

Described herein is a facile and efficient methodology toward the synthesis of Morusin scaffolds and Morusignin L scaffolds 4-9 and 12via a novel three-step approach (Michael addition or prenylation, cyclization and cyclization) and use a rapid, microwave-accelerated cyclization as the key step. Furthermore, their biological activities have been preliminarily demonstrated by in vitro evaluation for anti-osteoporosis activity. These Morusin, Morusignin L and newly synthesized compounds 5b, 6a, 8e, 8f greatly exhibited the highest potency, especially at the 10-5mol/L (P<0.01), and had good in vitro anti-osteoporosis activities using the commercially available standard drug Ipriflavone as a positive control. The mechanisms associated with anti-osteoporosis effects of these compounds may be through the inhibition of TRAP enzyme activity and bone resorption in osteoclasts, and promotion effect of osteoblast proliferation in vitro. The results indicated that Morusin scaffolds and Morusignin L scaffolds may be useful leads for further anti-osteoporosis activity screenings.

Corilagin attenuates aerosol bleomycin-induced experimental lung injury.

Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson's trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1ß, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-ß1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-ß1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis.

[Familial idiopathic pulmonary fibrosis: case report and review of literature].

OBJECTIVE: To investigate the clinical features of familial idiopathic pulmonary fibrosis (FIPF) and therefore to improve the recognition of the disease. METHODS: Clinical data of 5 patients with idiopathic pulmonary fibrosis belonging to 2 families were analyzed retrospectively. RESULTS: There were 3 patients in one family and 2 in another family. The average age at first diagnosis of the 5 patients with FIPF were (55 +/- 12) years. The most common initial symptoms were cough and progressive dyspnea, bibasilar end-inspiratory Velcro and clubbed fingers. HRCT revealed reticular opacities and diffuse honeycombing. Pulmonary ventilatory function was normal, but the diffusing capacity for carbon monoxide was reduced. One case was confirmed to have usual interstitial pneumonia by surgical lung biopsy. CONCLUSIONS: The clinical features of FIPF are similar to those of nonfamilial IPF. Asymptomatic FIPF can be identified early by lung HRCT.

[Cell apoptosis and the associated signal expression in epithelial cells from patients with idiopathic pulmonary fibrosis].

OBJECTIVE: To investigate the changes and significance of cell apoptosis, Fas/FasL and P53 protein in epithelial cells from patients with idiopathic pulmonary fibrosis (IPF). METHODS: Cell apoptosis and the expressions of Fas/FasL and P53 protein in lung tissues from 12 patients with IPF (IPF group) and 10 normal controls (control group) were detected by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) and immunohistochemistry. RESULTS: Compared with the control group (0/10), the percentage of apoptosis in alveolar epithelial cells and bronchial cells of the IPF group (12/12) was higher. The percentage of Fas, FasL and P53 protein expressions (12/12, 12/12, 11/12) in alveolar epithelial cells of the IPF group were higher than those of the control group (5/10, 2/10, 0/10); and the percentage of Fas, FasL and P53 protein expressions (12/12, 12/12, 11/12) in bronchial cells of the IPF group were also higher than those of the control group (6/10, 3/10, 0/10). There was a significant correlation between the percentage of apoptosis and Fas/FasL and P53 protein expression (r=0.625-0.839, all P<0.01). The correlation of the Fas/FasL and P53 protein expression was also significant (r=0.571-0.760, all P<0.01). CONCLUSION: The apoptosis percentage of epithelial cells and the expression of Fas/FasL and P53 protein are up-regulated in lung tissues of IPF, which may play an important role in the development of the disease.