Triptolide exposure triggers ovarian inflammation by activating cGAS-STING pathway and decrease oocyte quality in mouse.

Triptolide (TPL), a prominent bioactive constituent derived from the Chinese herb Tripterygium wilfordii, exhibits diverse pharmacological effects such as anti-tumor and anti-immune properties. Despite its extensive clinical application for the treatment of arthritis and immune disorders, TPL has been associated with multiorgan toxicity, including adverse effects on the female reproductive system. However, the precise mechanisms underlying TPL-induced ovarian damage remain poorly understood.

Acrolein exposure affects ovarian function by interfering with glycolysis and mitochondrial energy metabolism in mouse.

Acrolein is a widespread contaminant found in both diet and environment, entering the human body through food, alcohol, smoking, and exposure to fuel combustion fumes. While prior studies have highlighted acrolein's harmful impact on oocyte quality and early embryonic development in vitro, the specific mechanisms by which acrolein affects the female reproductive system in vivo remain poorly understood. This study first confirmed that in vitro acrolein exposure disrupts spindle morphology and chromosome alignment during the mid-MI stage of oocyte development, thus hindering oocyte maturation.

Asperuloside Promotes Apoptosis of Cervical Cancer Cells through Endoplasmic Reticulum Stress-Mitochondrial Pathway.

Objective: To investigate the effects of asperuloside on cervical cancer based on endoplasmic reticulum (ER) stress and mitochondrial pathway.

Methods: Different doses (12.5-800 µg/mL) of asperuloside were used to treat cervical cancer cell lines Hela and CaSki to calculate the half maximal inhibitory concentration (IC) of asperuloside.

Effects of sodium ferulate on amyloid-beta-induced MKK3/MKK6-p38 MAPK-Hsp27 signal pathway and apoptosis in rat hippocampus.

Aim: To observe the effects of sodium ferulate (SF) on amyloid beta (Abeta)1-40-induced p38 mitogen-activated protein kinase (MAPK) signal transduction pathway and the neuroprotective effects of SF.

Methods: Rats were injected intracerebroventricularly with Abeta1-40. Six hours after injection, Western blotting was used to determine the expressions of phosphorylated mitogen-activated protein kinase kinase (MKK) 3/MKK6, phospho-p38 MAPK, interleukin (IL)-1beta, phospho-MAPK activating protein kinase 2 (MAPKAPK-2), the 27 kDa heat shock protein (Hsp27), procaspase-9, -3, and -7 cleavage, and poly (ADP-ribose) polymerase (PARP) cleavage.

[Mechanism of cardioprotection against ischemia/reperfusion injury by valsartan: an experiment with isolated rat hearts].

Objective: To investigate the mechanism of protection of reperfused ischemic heart by valsartan.

Methods: The hearts of 40 SD rats were isolated, linked to Langendorff perfusion apparatus, and randomly divided into 5 equal groups: control group, to be perfused with modified Kreb-Henseleit (K-H) buffer for 110 minutes; ischemia/reperfusion (I/R) group, to be perfused with K-H buffer for 20 min, exposed to ischemia for 30 min, and then reperfused with K-H buffer for 60 min; HOE140 group, to be perfused with K-H buffer with HOE140, a bradykinin beta(2) receptor antagonist for 20 min, exposed to ischemia for 30 min, and then reperfused with K-H buffer with HOE140for 60 min; valsartan group, perfused with K-H buffer with valsartan for 20 min, exposed to ischemia for 30 min, and then reperfused with K-H buffer with valsartan for 60 min; and valsartan + HOE140 group, perfused with K-H buffer with valsartan + HOE140 for 20 min, exposed to ischemia for 30 min, and then reperfused with K-H buffer with valsartan + HOE140 for 60 min. The left ventricular systolic pressure (LVSP) and maximal uprising velocity of left ventricular pressure (+dp/dt(max)) were measured 20 minutes after the stabilization of perfusion, and 20, 40, and 60 minutes after reperfusion.

Sodium ferulate prevents amyloid-beta-induced neurotoxicity through suppression of p38 MAPK and upregulation of ERK-1/2 and Akt/protein kinase B in rat hippocampus.

Aim: To observe whether an amyloid beta (Abeta)-induced increase in interleukin (IL)-1beta was accompanied by an increase in the p38 mitogen-activated protein kinase (MAPK) pathway and a decrease in the cell survival pathway, and whether sodium ferulate (SF) treatment was effective in preventing these Abeta-induced changes.

Methods: Rats were injected intracerebroventricularly with Abeta25-35. Seven days after injection, immunohistochemical techniques for glial fibrillary acidic protein (GFAP) were used to determine the astrocyte infiltration and activation in hippocampal CA1 areas.