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Remote ischemic postconditioning protects against gastric mucosal lesions in rats
Tao Wang1, Ye-Ting Zhou1, Xin-Nian Chen1
1Tao Wang, Department of Anesthesiology, Shuyang People's Hospital, Shuyang 223600, Jiangsu Province, China.
Aim:
To investigate the protective effects of remote ischemic postconditioning (RIP) against limb ischemia-reperfusion (IR)-induced gastric mucosal injury.
Methods:
Gastric IR was established in male Wistar rats by placing an elastic rubber band under a pressure of 290-310 mmHg on the proximal part of both lower limbs for 3 h followed by reperfusion for 0, 1, 3, 6, 12 or 24 h. RIP was performed using three cycles of 30 s of reperfusion and 30 s of reocclusion of the femoral aortic immediately after IR and before reperfusion for up to 24 h. Rats were randomly assigned to receive IR (n = 36), IR followed by RIP (n = 36), or sham treatment (n = 36). Gastric tissue samples were collected from six animals in each group at each timepoint and processed to determine levels of malondialdehyde (MDA), superoxide dismutase (SOD), xanthine oxidase (XOD) and myeloperoxidase (MPO). Additional samples were processed for histologic analysis by hematoxylin and eosin staining. Blood samples were similarly collected to determine serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), tumor necrosis factor (TNF)-α and interleukin (IL)-10.
Results:
The pathologic changes in gastric tissue induced by IR were observed by light microscopy. Administration of RIP dramatically reduced the gastric damage score after 6 h of reperfusion (5.85 ± 0.22 vs 7.72 ± 0.43; P < 0.01). In addition, RIP treatment decreased the serum activities of LDH (3.31 ± 0.32 vs 6.46 ± 0.03; P < 0.01), CK (1.94 ± 0.20 vs 4.54 ± 0.19; P < 0.01) and the concentration of TNF-α (53.82 ± 0.85 vs 88.50 ± 3.08; P < 0.01), and elevated the concentration of IL-10 (101.46 ± 5.08 vs 99.77 ± 4.32; P < 0.01) induced by IR at 6 h. Furthermore, RIP treatment prevented the marked elevation in MDA (3.79 ± 0.29 vs 6.39 ± 0.81) content, XOD (7.81 ± 0.75 vs 10.37 ± 2.47) and MPO (0.47 ± 0.05 vs 0.82 ± 0.03) activities, and decrease in SOD (4.95 ± 0.32 vs 3.41 ± 0.38; P < 0.01) activity in the gastric tissue as measured at 6 h.
Conclusion:
RIP provides effective functional protection and prevents cell injury to gastric tissue induced by limb IR via anti-inflammatory and antioxidant actions.
Insights
Remote ischemic postconditioning (RIP) effectively protects gastric tissue from limb ischemia-reperfusion (IR) injury. This method reduces inflammation and oxidative stress, preserving gastric mucosal integrity.
Area of Science:
- Physiology
- Pathology
- Medical Research
Background:
- Limb ischemia-reperfusion (IR) injury can cause significant damage to remote organs, including the gastric mucosa.
- Understanding protective mechanisms against IR-induced injury is crucial for clinical interventions.
Purpose of the Study:
- To investigate the protective effects of remote ischemic postconditioning (RIP) against limb IR-induced gastric mucosal injury in a rat model.
- To evaluate the impact of RIP on biochemical markers and histological changes in gastric tissue.
Main Methods:
- Gastric IR was induced in male Wistar rats.
- RIP was applied using cycles of femoral artery occlusion and reperfusion immediately after IR.
- Gastric tissue and blood samples were analyzed for markers of oxidative stress, inflammation, and cell injury.
Main Results:
- RIP significantly reduced gastric damage scores and improved histological findings.
- RIP treatment decreased serum lactate dehydrogenase (LDH), creatine kinase (CK), and tumor necrosis factor-alpha (TNF-α) levels.
- RIP prevented the increase in malondialdehyde (MDA) and xanthine oxidase (XOD) activities, and the decrease in superoxide dismutase (SOD) activity in gastric tissue.
Conclusions:
- Remote ischemic postconditioning (RIP) offers effective functional protection against limb IR-induced gastric mucosal injury.
- RIP exerts its protective effects through anti-inflammatory and antioxidant mechanisms.
- RIP is a promising therapeutic strategy for mitigating organ damage following IR events.
