Journal of Traditional and Complementary Medicine最新文献

Background and aim

Experimental procedure

Results and conclusion

Background

Methods

Results and conclusion

Background and aim

Experimental procedure

Results and conclusion

Purpose

Methods

Results

Conclusions

The Traditional Chinese Medicine compound preparation known as Diwu Yanggan capsule (DWYG) can effectively hinder the onset and progression of hepatocellular carcinoma (HCC), which is recognized worldwide as a significant contributor to fatalities associated with cancer. Nevertheless, the precise mechanisms implicated have remained ambiguous. In present study, the model of HCC was set up by the 2-acetylaminofluorene (2-AAF)/partial hepatectomy (PH) in rats. To confirm the differentially expressed genes (DEGs) identified in the microarray analysis, real-time quantitative reverse transcription PCR (qRT-PCR) was conducted. In the meantime, the liquid chromatography-quadrupole time of flight mass spectrometry (LC-QTOF-MS/MS) was employed to characterize the component profile of DWYG. Consequently, the DWYG treatment exhibited the ability to reverse 51 variation genes induced by 2-AAF/PH. Additionally, there was an overlap of 54 variation genes between the normal and model groups. Upon conducting RT-qPCR analysis, it was observed that the expression levels of all genes were increased by 2-AAF/PH and subsequently reversed after DWYG treatment. Notably, the fold change of expression levels for all genes was below 0.5, with 3 genes falling below 0.25. Moreover, an investigation was conducted to determine the signaling pathway that was activated/inhibited in the HCC group and subsequently reversed in the DWYG group. Moreover, the component profile of DWYG encompassed a comprehensive compilation of 206 compounds that were identified or characterized. The findings of this study elucidated the potential alleviative mechanisms of DWYG in the context of HCC, thereby holding significant implications for its future clinical utilization and widespread adoption.

Background and aim

Hypoxia of the cartilage has been considered as a potential pathogenic factor in knee osteoarthritis (KOA). Studies have shown that impaired blood perfusion of joint leads to cartilage hypoxia. Electroacupuncture (EA) has proven effects on pain relief and improving microcirculation. This study aimed to explore the effect of EA on articular microcirculation and cartilage anoxic and the underlying mechanisms.

Procedures

Videman's method was used for 6 weeks to establish the KOA model. EA intervention was performed in four points around the knee for 3 weeks after KOA modeling. The Lequesne MG score was used to assess ethology. We recorded the oxygen tension of synovial fluid and the synovial microcirculation in vivo. HE-staining was used to assess cartilage morphology, and immunohistochemistry (IHC), Western blotting, and RT-PCR were used to assess expression of the major glycolytic enzymes glucosetransporter1 (GLUT1), pyruvate kinase M2(PKM2), and lactate dehydrogenase A (LDHA). Enzyme-linked immunosorbent assay (Elisa) was used to detect lactate content.

Results and conclusion

There was a significant decrease in Lequesne MG score and improvement in Mankin score after EA intervention (P < 0.01), a significant increase in synovial microcirculation (P < 0.05) and synovial fluid oxygen tension (P < 0.01), and there was significant decrease in the expression of GLUT1, PKM2 and LDHA (P < 0.01) and lactate (P < 0.05). This study suggested that EA ameliorate cartilage hypoxia and regulate glycolytic metabolism in chondrocytes in KOA model rabbits by improving articular microcirculation and oxygen tension.

STRP1, a polysaccharide active ingredient isolated from the traditional Chinese medicine Sophorae tonkinensis radix, has demonstrated a protective effect against acetaminophen (APAP)-induced liver injury (AILI). The underlying molecular mechanism was investigated in this study. Here, an acute liver damage mouse model was generated by APAP (400 mg/kg) and used to identify the protective effect of STRP1 (200 mg/kg) on mouse livers. In vitro cell experiments were used to further verify the related signaling pathways. Initially, in our study, STRP1 treatment reduced APAP-induced liver injury by decreasing aminotransferase activity and cell apoptosis and increasing cell proliferation. Furthermore, STRP1 treatment significantly increased Nrf2 expression and alleviated oxidative stress caused by reactive oxygen species in AILI. Based on bioinformatics and experimental studies, miR-140-5p was identified and found to be reduced by STRP1, increasing Nrf2 expression. Additionally, Nrf2 played an important role in the protective impact of STRP1-suppressed miR-140-5p expression. Generally, these results showed that STRP1-mediated suppression of miR-140-5p expression mitigates AILI by activating the Nrf2-mediated Nrf2-Keap1 pathway. This study revealed that STRP1 might be a potential treatment agent for AILI.

Background and aim

Type-2 diabetes mellitus (T2DM) is mainly characterized by insulin resistance (IR) induced by hyperglycaemia and insufficient insulin secretion. We employed a diabetic fly model to examine the effect and molecular mechanism of Atractylodes macrocephala Koidz. and Cuscuta chinensis Lam. (AMK–CCL) extract as traditional Chinese medicine in treating IR and T2DM.

Experimental procedure

The contents of the active ingredients (rhamnose, xylose, mannose, and hyperoside) in AMK–CCL extract were determined by high-performance liquid chromatography. Wild-type (Cg-GAL4/+) or diabetic (Cg > InR^K1409A) Drosophila flies were divided into the control group or metformin group and AMK–CCL (0.0125, 0.025, 0.05, 0.1 g/ml) groups. Food intake, haemolymph glucose and trehalose, protein, weight, triglycerides (TAG), and glycogen were measured to assess glycolipid metabolism. Phosphatidylinositol-3-kinase (PI3K)/Akt signalling was detected using fluorescent reporters [tGPH, Drosophila forkhead box O (dFoxO)–green fluorescent protein (GFP), Glut1–GFP, 2-NBDG] in vivo. Glut1/3 mRNA levels and Akt phosphorylation levels were detected by quantitative polymerase chain reaction and western blotting, respectively, in vitro.

Results

AMK–CCL extract contained 0.038 % rhamnose, 0.017 % xylose, 0.69 % mannose, and 0.039 % hyperoside. AMK–CCL at 0.0125 g/mL significantly suppressed the increase in circulating glucose, and the decrease in body weight, TAG, and glycogen contents of diabetic flies. AMK–CCL improved PI3K activity, Akt phosphorylation, Glut1/3 expression, and glucose uptake in diabetic flies, and also rescued diabetes-induced dFoxO nuclear localisation.

Conclusions

These findings indicate that AMK–CCL extract ameliorates IR-induced diabetes via the PI3K/Akt signalling pathway, providing an experimental basis for clinical treatment.