ABSTRACT
BACKGROUND: Skeletal muscle ischaemia-reperfusion injury (IRI) is a prevalent condition encountered in clinical practice, characterised by muscular dystrophy. Owing to limited treatment options and poor prognosis, it can lead to movement impairments, tissue damage, and disability. This study aimed to determine and verify the influence of transient receptor potential canonical 6 (TRPC6) on skeletal muscle IRI, and to explore the role of TRPC6 in the occurrence of skeletal muscle IRI and the signal transduction pathways activated by TRPC6 to provide novel insights for the treatment and intervention of skeletal muscle IRI. METHODS: In vivo ischaemia/reperfusion (I/R) and in vitro hypoxia/reoxygenation (H/R) models were established, and data were comprehensively analysed at histopathological, cellular, and molecular levels, along with the evaluation of the exercise capacity in mice. RESULTS: By comparing TRPC6 knockout mice with wild-type mice, we found that TRPC6 knockout of TRPC6 could reduced skeletal muscle injury after I/R or H/R, of skeletal muscle, so as therebyto restoringe some exercise capacity inof mice. TRPC6 knockdown can reduced Ca2+ overload in cells, therebyo reducinge apoptosis. In additionAdditionally, we also found that TRPC6 functionsis not only a key ion channel involved in skeletal muscle I/R injury, but also can affects Ca2+ levels and then phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signalling pathway. by knocking downTherefore, knockdown of TRPC6, so as to alleviated the injury inducedcaused by skeletal muscle I/R or and H/R. CONCLUSIONS: These findingsdata indicate that the presence of TRPC6 exacerbatescan aggravate the injury of skeletal muscle injury after I/Rischemia/reperfusion, leading towhich not only causes Ca2+ overload and apoptosis., Additionally, it impairsbut also reduces the self- repair ability of cells by inhibiting the expression of the PI3K/Akt/mTOR signalling pathway. ETo exploringe the function and role of TRPC6 in skeletal muscle maycan presentprovide a novelew approachidea for the treatment of skeletal muscle ischemia/reperfusion injury.
Subject(s)
Apoptosis , Mice, Knockout , Muscle, Skeletal , Reperfusion Injury , Signal Transduction , TRPC6 Cation Channel , Animals , Reperfusion Injury/metabolism , Reperfusion Injury/pathology , TRPC6 Cation Channel/metabolism , TRPC6 Cation Channel/genetics , Muscle, Skeletal/metabolism , Muscle, Skeletal/pathology , Mice , Mice, Inbred C57BL , Proto-Oncogene Proteins c-akt/metabolism , TOR Serine-Threonine Kinases/metabolism , Male , Phosphatidylinositol 3-Kinases/metabolism , Calcium/metabolismABSTRACT
Time-of-death extrapolation has always been one of the most important issues in forensic practice. For a complicated case in which a corpse is destroyed with little evidence, judging the time of death of the deceased is a major challenge, which also enables criminals to escape legal sanctions. To find a method to roughly judge the time of death of a corpse with only a small amount of skin tissue, in this study, we established an early death model by using mice; furthermore, the postmortem interval was estimated by determining the protein and mRNA levels of Bax and Bcl-2 in the skin. In this process, 0 h after death was used as the control group, and the expression levels of Bax and Caspase-3 reached the maximum value at 8-12 h, while Bcl-2, as an inhibitor of apoptosis protein, peaked after 24 h. The mRNA expression levels of related proteins in postmortem skin tissues were also different. The results of these data indicate that the protein and mRNA levels of Bax and Bcl-2 in the skin have potential application in early time-of-death estimation.
ABSTRACT
In this article, influence of monocalcium phosphate and potassium chloride application on nitrogen leaching in paddy soil of Taihu region was studied by soil column leaching. The results showed that nitrate nitrogen was the main component of nitrogen leaching without urea application which accounts for 93.39 percent of total nitrogen leaching (including urea, ammonium, and nitrate nitrogen). Amounts of urea, ammonium, and nitrate nitrogen in leachates increased significantly after urea application which account for 3.95, 15.25, and 80.80 percent of total nitrogen leaching respectively and for 0.26, 0.80, and 2.54 percent of applied nitrogen respectively. Amounts of urea, ammonium, and nitrate nitrogen in leachates were enhanced prominently by monocalcium phosphate or potassium chloride which are 4.54, 24.11, 71.34, and 3.45, 24.53, 72.02 percent of total nitrogen leaching respectively, and which are 0.39, 1.86, 3.34, and 0.32, 2.12, 4.06 percent of applied nitrogen separately. There is interactive influence on nitrogen leaching after application of monocalcium phosphate and potassium chloride together, and amounts of urea, ammonium, and nitrate nitrogen were 4.10, 27.35, and 68.55 percent of total nitrogen leaching, and 0.42, 2.60, and 4.26 percent of total applied nitrogen respectively. The leaching order of different form nitrogen followed as urea N > ammonium N > nitrate N, and leaching amounts of different form nitrogen followed as urea N < ammonium N < nitrate N.