| Sample Type | n | Range | Average |
|---|---|---|---|
| Serum | 5 | 85% - 103% | 93% |
| EDTA Plasma | 5 | 86% - 104% | 95% |
| Heparin Plasma | 5 | 88% - 104% | 94% |
| Sample Type | n | 1:2 | 1:4 | 1:8 |
|---|---|---|---|---|
| Serum | 5 | 85-104% | 88-103% | 87-104% |
| EDTA Plasma | 5 | 87-101% | 84-100% | 82-99% |
| Heparin Plasma | 5 | 87-100% | 90-93% | 82-99% |
| Item | Quantity | Storage |
|---|---|---|
| Pre-Coated 96 Well Microplate | 12 x 8 Well Strips | +4°C |
| Lyopholized Standard | 2 Vials | +4°C |
| Sample Dilution Buffer | 20ml | +4°C |
| Biotinylated Detection Antibody | 120µl | +4°C |
| Antibody Dilution Buffer | 10ml | +4°C |
| HRP-Streptavidin Conjugate | 120µl | +4°C |
| SABC Dilution Buffer | 10ml | +4°C |
| TMB Substrate | 10ml | +4°C |
| Stop Solution | 10ml | +4°C |
| Wash Buffer (25X) | 30ml | +4°C |
| Plate Sealers | 5 Adhesive Strips | - |
| Foil Pouch | 1 Zip-Sealed Pouch | - |
Background: Hepatic ischemia-reperfusion injury (HIRI) remains one of the major causes of postoperative liver dysfunction following extensive hepatectomy and liver transplantation. Owing to its progressive and dynamic nature, HIRI may lead to multiple organ failure and a worsened outcome. Treprostinil is a relatively new synthetic prostacyclin analog with a potential beneficial effect against HIRI. Ischemic preconditioning (IP) is a promising method to protect against HIRI.
Aim: To investigate HIRI biomarkers, their effects on liver and heart, and the effects of treprostinil and IP on these processes.
Methods: Forty male Wistar albino rats aged 3-4 months were randomly assigned to four groups of ten, subjected to a 3-hour surgical intervention, and then sacrificed. Hepatic ischemia was induced by clamping the hepatoduodenal ligament for 30 minutes, followed by reperfusion for 120 minutes. Treprostinil (100 ng/kg/minute for 24 hours) or IP before HIRI, no protection, and a sham operation were applied accordingly in each group. Liver and heart histopathology and specific serum and hepatic tissue biomarkers were assessed.
Results: HIRI deteriorated hepatocellular function and exacerbated liver and myocardial damage in the control group. Furthermore, HIRI triggered cytokine overexpression and protein carbonyl content (P < 0.001). Compared with those in the HIRI group, lower troponin I, tumor necrosis factor-a, endothelin-1, and interleukin-1ß in serum and liver tissue were significantly correlated with reduced cellular necrosis and improved hepatocellular function in the treprostinil group (P < 0.001). Similar but less pronounced effects were observed in the IP group. Both treprostinil and IP had protective effects in hepatic and cardiac tissues. However, treprostinil showed slightly superior cardioprotective efficacy, as evidenced by a statistically significant difference in troponin I levels (P < 0.05) and histopathological scoring of myocardium samples, but there were no differences in the other parameters.
Conclusion: HIRI results in oxidative stress and cytokine overexpression, which deteriorate hepatic function and accelerates myocardial damage. Treprostinil and IP are promising strategies for preventing reperfusion-induced cellular and systemic damage.
This study evaluated the cardioprotective effects of Alpinia galanga rhizome extract (GRE) against noise-induced myocardial injury via phytochemical profiling, molecular docking, and in vivo assessment. Male Wistar rats (n = 6/group) were assigned to the following four groups: control (C), control + GRE (100 mg/kg), noise-exposed (N), and noise-exposed + GRE (N+GRE, 100 mg/kg). Rats in the N and N+GRE groups were exposed to 90 dB(A) white noise for 2 h/day for 28 days, with GRE administered orally throughout the exposure period. Phytochemical analysis confirmed the presence of flavonoids and phenolic acids with known antioxidant and anti-inflammatory activities. In vitro, GRE significantly reduced nitric oxide production in lipopolysaccharide-stimulated RAW264.7 macrophages. In vivo, noise exposure elevated cardiac malondialdehyde levels, impaired antioxidant enzyme activity, and increased circulating tumor necrosis factor-alpha (TNF-a) and heme oxygenase-1 (HO-1) levels. GRE treatment restored redox balance, suppressed proinflammatory mediator levels, and improved histopathological alterations. Molecular docking analysis indicated strong binding of GRE phytoconstituents to HO-1 and TNF-a, supporting the observed in vivo effects. These findings demonstrate that GRE mitigates noise-induced cardiac injury through its antioxidant and anti-inflammatory properties, highlighting its therapeutic potential.
