Efficacy and safety of Mahuang Fuzi and Shenzhuo Decoction for treatment of primary membranous nephropathy: a multicenter prospective trial.

BACKGROUND: This study aims to undertake a comprehensive assessment of the effectiveness and safety profile of Mahuang Fuzi and Shenzhuo Decoction (MFSD) in the management of primary membranous nephropathy (PMN), within the context of a prospective clinical investigation. METHODS: A multicenter, open-label clinical trial was executed on patients diagnosed with PMN. These individuals were subjected to MFSD therapy for a duration of at least 24 months, with primary outcome of clinical remission rates. The Cox regression analysis was employed to discern the pertinent risk factors exerting influence on the efficacy of MFSD treatment, with scrupulous monitoring of any adverse events. RESULTS: The study comprised 198 participants in total. Following 24 months of treatment, the remission rate was 58.6% (116/198). Among the subgroup of 130 participants subjected to a 36-month follow-up, the remission rate reached 70% (91/130). Subgroup analysis revealed that neither a history of immunosuppressive therapy (HIST) nor an age threshold of ≥60 years exhibited a statistically significant impact on the remission rate at the 24-month mark (p > .05). Multivariate Cox regression analyses elucidated HIST, nephrotic syndrome, or mass proteinuria, and a high-risk classification as noteworthy risk factors in the context of MFSD treatment. Remarkably, no fatalities resulting from side effects were documented throughout the study's duration. CONCLUSIONS: This trial establishes the efficacy of MFSD as a treatment modality for membranous nephropathy. MFSD demonstrates a favorable side effect profile, and remission rates are consistent across patients, irrespective of HIST and age categories.

EGCG evokes Nrf2 nuclear translocation and dampens PTP1B expression to ameliorate metabolic misalignment under insulin resistance condition.

As a major nutraceutical component of green tea (-)-epigallocatechin-3-gallate (EGCG) has attracted interest from scientists due to its well-documented antioxidant and antiobesity bioactivities. In the current study, we aimed to investigate the protective effect of EGCG on metabolic misalignment and in balancing the redox status in mice liver and HepG2 cells under insulin resistance condition. Our results indicated that EGCG accelerates the glucose uptake and evokes IRS-1/Akt/GLUT2 signaling pathway via dampening the expression of protein tyrosine phosphatase 1B (PTP1B). Consistently, ectopic expression of PTP1B by Ad-PTP1B substantially impaired EGCG-elicited IRS-1/Akt/GLUT2 signaling pathway. Moreover, EGCG co-treatment stimulated nuclear translocation of Nrf2 by provoking P13K/AKT signaling pathway and thus modulated the downstream expressions of antioxidant enzymes such as HO-1 and NQO-1 in HepG2 cells. Furthermore, knockdown Nrf2 by small interfering RNA (siRNA) notably enhanced the expression of PTP1B and blunt EGCG-stimulated glucose uptake. Consistent with these results, in vivo study revealed that EGCG supplement significantly ameliorated high-fat and high-fructose diet (HFFD)-triggered insulin resistance and oxidative stress by up-regulating the IRS-1/AKT and Keap1/Nrf2 transcriptional pathways. Administration of an appropriate chemopreventive agent, such as EGCG, could potentially serve as an additional therapeutic intervention in the arsenal against obesity.

Neuroprotective action of tea polyphenols on oxidative stress-induced apoptosis through the activation of the TrkB/CREB/BDNF pathway and Keap1/Nrf2 signaling pathway in SH-SY5Y cells and mice brain.

Many studies have shown that oxidative stress is a major cause of cellular injuries in a variety of human diseases including cognitive impairment. Tea polyphenols (TPs), natural plant flavonoids found in tea plant leaves, possess the bioactivity to affect the pathogenesis of several chronic diseases via antioxidant associated mechanisms. However, the possible antioxidant and neuroprotective properties of TPs in the brain of mice housed in constant darkness and in H2O2-stimulated SH-SY5Y cells are yet to be elucidated. In this study, pretreatment with TPs markedly attenuated H2O2-elicited cell viability loss and mitochondrial dysfunction, suppressed the induced apoptosis and reduced the elevated levels of intracellular ROS and H2O2. Additionally, TPs modulate the nuclear translocation of Nrf2 and the TrkB/CREB/BDNF signaling pathway by provoking the PI3K/AKT pathway and thus, they transcriptionally regulate the downstream expression of antioxidant enzymes including HO-1, NQO-1, and BDNF in SH-SY5Y cells. Furthermore, an in vivo study revealed that housing mice in constant darkness, simulating shift work disruption in humans, notably affects the AKT/CREB/BDNF signal pathway and the nuclear translocation of Nrf2 and its downstream phase II detoxification enzymes in brain tissue. Remarkably, TP supplementation through drinking water eliminated these changes. These results suggest that TPs possess protective effects against oxidative stress-triggered cognitive impairment, which might be a potential nutritional preventive strategy for neurodegenerative diseases implicated with oxidative stress in shift workers.

[The quality standard study on Hugan qingzhi tablets].

OBJECTIVE: To develop a method of quality control for Hugan qingzhi tablets. METHODS: Fructus Crataegi, Rhizoma Alismatis and Radix Notoginseng were identified by TLC. HPLC was used for the determination of ursolic acid in Hugan qingzhi tablets. RESULTS: The chromatographic spots were identified without the interference of negative control. Ursolic acid had a good linearity over the concentration range of 40-200 microg/mL (r = 1.000). The average recoveries was 99.05% with relatively standard deviations of 1.3%. CONCLUSION: This method is reliable, accurate and specific and can be used for the quality control of Hugan qingzhi tablets.