Portal hypertension produces an evolutive hepato-intestinal pro- and anti-inflammatory response in the rat

Procalcitonin, and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites

“…Consistent with these facts, it known that oral medications such as cisapride and trimethoprim-sulfamethoxazole can attenuate bacterial overgrowth, enhance mucosal function, and increase intestinal transit, all leading to reduced rates of BT [13][14][15] . Even in the absence of overt infection, there is a significant inflammatory response in cirrhotic patients occurring as a result of a complex interaction of pro-and anti-inflammatory cytokines consisting of numerous interleukins, tumor necrosis factor-alpha (TNF-α), interferon gamma (IFNγ) and complement proteins [16][17][18] . This concerted cytokine response has both temporal and site specific properties in cirrhotic patients with portal hypertension [16,17] .…”

“…Even in the absence of overt infection, there is a significant inflammatory response in cirrhotic patients occurring as a result of a complex interaction of pro-and anti-inflammatory cytokines consisting of numerous interleukins, tumor necrosis factor-alpha (TNF-α), interferon gamma (IFNγ) and complement proteins [16][17][18] . This concerted cytokine response has both temporal and site specific properties in cirrhotic patients with portal hypertension [16,17] . One particular inflammatory marker is procalcitonin (PCT), a 116 amino acid protein made in multiple sites of the body including liver and intestine.…”

Effects and Interactions of Ginger and Propranolol in Pre-Hepatic Portal Hypertensive Rats

“…This effect might be attributed to reduction of NO and PG production within the splanchnic circulation. [31] Moreover, ginger could decrease the inflammatory mediators like TNF-α, interleukin-1β (IL-1β), carbon monoxide (CO) and IL-10 [25]. In the same context, the potential antimicrobial effect of ginger [32] as well as inhibition of angiogenesis [33] could share in the reduction of portal pressure.…”

“…Proand anti-inflammatory mediators like nitric oxide (NO) and tumor necrosis factor α (TNF-α), are released from the gut and the liver in PHT [25]. NO and its possible interaction with prostaglandin I 2 (PGI 2 ) Marked (cellular infiltration, congested tortuous blood vessels in mucosa and sub-mucosa with edema, erosion).…”

“…These results are in agreement with Sigala et al [36] who reported that sympathetic nervous system (SNS) signaling regulates hepatic fibrogenesis through effects on hepatic stellate cells (HSC), in which SNS activation accelerates progression of NAFLD. PHT in rat shows persistent splanchnic alterations related to the elevated pressure and produces changes in the metabolism of lipids and carbohydrates that could be involved in the development of liver steatosis [25].…”