Comparison of anesthesia quality between desflurane, sevoflurane, and propofol in elderly patients undergoing laparoscopic cholecystectomy during and after surgery

Start Date01 Jul 2024

Sponsor / Collaborator

Tianjin Nankai Hospital

ChiCTR2400080454 / SuspendedPhase 4IIT

Effect of oxycodone hydrochloride injection in patients diagnosed with sepsis induced acute lung injury

Start Date01 Apr 2024

Sponsor / Collaborator

Tianjin Nankai Hospital

ChiCTR2400082542 / SuspendedNot ApplicableIIT

Observational study on the lung protective effect of remifentanil based on driving pressure in ICU mechanically ventilated patients

Start Date01 Apr 2024

Sponsor / Collaborator

Tianjin Nankai Hospital

100 Clinical Results associated with Tianjin Nankai Hospital

0 Patents (Medical) associated with Tianjin Nankai Hospital

726

Literatures (Medical) associated with Tianjin Nankai Hospital

31 Dec 2024·Pharmaceutical Biology

Nicotinamide mononucleotide alleviates endotoxin-induced acute lung injury by modulating macrophage polarization via the SIRT1/NF-κB pathway

Article

Author: Yang, Jing ; Dong, Shuan ; Zhang, Yuan ; Du, Shihan ; Gong, Lirong ; Jiang, Xianhong ; He, Simeng ; Wu, Xiaoyang ; Shi, Jia ; Yu, Jianbo ; Wu, Ya

CONTEXTSepsis-induced acute lung injury (ALI) is a severe condition with limited effective therapeutics; nicotinamide mononucleotide (NMN) has been reported to exert anti-inflammatory activities.OBJECTIVEThis study explores the potential mechanisms by which NMN ameliorates sepsis-induced ALI in vivo and in vitro.MATERIALS AND METHODSCultured MH-S cells and a murine model were used to evaluate the effect of NMN on sepsis-induced ALI. MH-S cells were stimulated with LPS (1 μg/mL) and NMN (500 μM) for 12 h grouping as control, LPS, and LPS + NMN. Cell viability, apoptotic status, and M1/2 macrophage-related markers were detected. The mice were pretreated intraperitoneally with NMN (500 mg/kg) and/or EX-527 (5 mg/kg) 1 h before LPS injection and randomized into 7 groups (n = 8): control, LPS, LPS + NMN, NMN, LPS + NMN + EX-527 (a SIRT1 inhibitor), LPS + EX-527, and EX-527. After 12 h, lung histopathology, W/D ratio, MPO activity, NAD⁺ and ATP levels, M1/2 macrophage-related markers, and expression of the SIRT1/NF-κB pathway were detected.RESULTSIn MH-S cells, NMN significantly decreased the apoptotic rate from 12.25% to 5.74%. In septic mice, NMN improved the typical pathologic findings in lungs and reduced W/D ratio and MPO activity, but increased NAD⁺ and ATP levels. Additionally, NMN suppressed M1 but promoted M2 polarization, and upregulated the expression of SIRT1, with inhibition of NF-κB-p65 acetylation and phosphorylation. Furthermore, inhibition of SIRT1 reversed the effects of NMN-induced M2 macrophage polarization.CONCLUSIONSNMN protects against sepsis-induced ALI by promoting M2 macrophage polarization via the SIRT1/NF-κB pathway, it might be an effective strategy for preventing or treating sepsis-induced ALI.

01 Jul 2024·Combinatorial Chemistry & High Throughput Screening

Protective Effects of Liriodendrin on Myocardial Infarction-Induced Fibrosis in Rats via the PI3K/Akt Autophagy Pathway: A Network Pharmacology Study

Article

Author: Zhuo, Yuzhen ; Lu, Yanmin ; Yang, Lei ; Li, Dihua ; Liu, Xuanming ; Yu, Xin ; Zhang, Ping

Background:Liriodendrin (LIR) has been reported to improve cardiac function in rats following myocardial infarction. However, its role and mechanism in reparative myocardial fibrosis remain unclear.Methods:In this study, a rat model of myocardial fibrosis was established via left anterior descending artery ligation and randomly divided into three groups (n = 6 per group): sham-operated, myocardial infarction, and LIR intervention (100 mg/kg/day) groups. The pharmacological effects of LIR were assessed using echocardiography, hematoxylin, and eosin (H&E) staining, and Masson staining. Network pharmacology and bioinformatics were utilized to identify potential mechanisms of LIR, which were further validated via western blot analysis.Results:Our findings demonstrated that LIR improved cardiac function, histology scores, and col lagen volume fraction. Moreover, LIR downregulated the expression of Beclin-1, LC3-II/LC3-I while upregulating the expression of p62, indicating LIR-inhibited autophagy in the heart after myocardial infarction. Further analysis revealed that the PI3K/Akt signaling pathway was significantly enriched and validated by western blot. This analysis suggested that the ratios of p- PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR were significantly increased.Conclusion:LIR may attenuate myocardial infarction-induced fibrosis in rats by inhibiting excessive myocardial autophagy, with the potential mechanism involving the activation of the PI3K/Akt/mTOR pathway.

01 Jun 2024·Naunyn-Schmiedeberg's Archives of Pharmacology

Antitumor effect of tubeimoside-I on murine colorectal cancers through PKM2-dependent pyroptosis and immunomodulation

Article

Author: Hu, Dongsheng ; Wang, Ximo ; Zhang, Sijia ; Wang, Yanli ; He, Siqi ; Li, Dihua ; Zhang, Lanqiu ; Cui, Lingzhi ; Zhuo, Yuzhen ; Yang, Lei

Induction of cancer cell death is an established treatment strategy, but chemotherapy drug-mediated apoptosis can be evaded by many tumors. Pyroptosis is a type of inflammatory programmed cell death (PCD) that is important for organism immunity. Tubeimoside-I (TBMS1) is a plant-derived component that exhibits antitumor activity. However, it is unclear how TBMS1 induces pyroptosis to inhibit colorectal cancer (CRC). In this study, we demonstrated that TBMS1 is able to induce pyroptosis in murine CRC cells and releases pro-inflammatory cytokines. Mechanistically, we found that TBMS1 inhibits CRC cell proliferation and migration and induces pyroptosis by activating caspase-3 and cleaving gasdermin E (GSDME) through the inhibition of PKM2. In the animal experiments, TBMS1 attenuated the weight of solid tumors, increased the proportion of CD8⁺ cytotoxic T cells, and reduced the content of M2-type macrophages in the spleen of tumor-bearing mice. Furthermore, TBMS1 inhibited M2-type polarization by blocking STAT6 pathway activation in RAW 264.7 cells. To sum up, our findings suggest that TBMS1 triggers pyroptosis in CRC by acting on the PKM2/caspase-3/GSDME signaling pathway. Additionally, it modulates the antitumor immune response in CRC murine models. This study provides a promising basis for the potential use of TBMS1 in treating CRC.

100 Deals associated with Tianjin Nankai Hospital

100 Translational Medicine associated with Tianjin Nankai Hospital

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