Overexpression of heat shock protein 70 and its relationship to intestine under acute heat stress in broilers: 2. Intestinal oxidative stress

Abstract

Oxidative stress injury is one important factor in intestinal mucosal barrier damage. Expression of heat shock protein (HSP)70 is an endogenous mechanism by which living cells adapt to stress. This study was undertaken to investigate the protective effects of HSP70 on intestinal oxidative stress. Two hundred and forty broilers were injected intraperitoneally with HSP70 inducer l-(1)-glutamine or with the inhibitor quercetin. Twenty-four hours later, they were heat stressed for 0, 2, 3, 5, and 10 h, respectively, at 36 ± 1°C. The l-(1)-glutamine significantly increased HSP70 expression (P < 0.001). At 2 h or 3 h of heat stress, the HSP70 expression obviously elevated (P < 0.001). Levels of corticosterone and the heterophil:lymphocyte ratio significantly increased when HSP70 expression was inhibited (P < 0.0001). Serum corticosterone was negatively correlated with the HSP70 expression at 3 h of heat stress (P = 0.0015; R = -0.6537). Heat shock protein 70 significantly protected the integrity of the intestinal mucosa from heat stress, with significantly decreased lactic dehydrogenase when HSP70 expression was enhanced (P < 0.001). In addition, heat-stress time significantly affected the lactic dehydrogenase release (P < 0.001). Furthermore, HSP70 significantly elevated antioxidant enzyme activities (such as superoxide dismutase, glutathione peroxidase, and total antioxidant capacity) and inhibited lipid peroxidation to relieve intestinal mucosal oxidative injury (P < 0.001). These results suggest that HSP70 is capable of protecting the intestinal mucosa from heat-stress injury by improving antioxidant capacity of broilers and inhibiting the lipid peroxidation production.

Upregulation of TLR4 mRNA Expression Levels in Broiler Chickens Under Acute Heat Stress

“…Fukata & Abreu (2007) demonstrated that TLR4 induces the activation of cyclooxygenase 2 and prostaglandin E2 in vitro and in vivo, which are important for cell proliferation and apoptosis in response to intestinal mucosal injury. Gu et al (2012) indicated that HSP70 is capable of protecting the intestinal mucosa from heat stress injury by enhancing the antioxidant capacity of broilers. Furthermore, TLR4 is involved in the recognition of endogenous or exogenous products of microbes, such as heat shock protein (HSP) and lipopolysaccharide (LPS) (Ohashi et al, 2000;Vabulas et al, 2001).…”

“…In addition, data from HS and endotoxin shock models (Ryan et al, 1994) support the critical role of the liver in the response to thermal and endotoxin challenge. During HS, a disturbance in the microecological balance of the intestinal flora may cause bacterial translocation and induce the production of intestinal endotoxins (Gu et al, 2012;Yu et al, 2013), allowing large amounts of endotoxins to reach the liver. TLR4 is stably expressed on the surface of many cells, including the Kupffer cells of the liver (Zuo et al, 2003).…”

Combined supplementation of organic acid blend and mannanoligosaccharide suppresses expression of heat shock protein 70 in broilers

“…They act as cytoprotective proteins and are having the ability to upsurge stress tolerance and enhance survival rates of heat stressed birds (Latchman, 2001). It has been reported that HSP mRNA expression is increased in birds that are exposed to stress rather than those that are kept at thermoneutral zone (Gu et al, 2012). It has also been reported that some supplementations can also regulate expression of HSP (Sahin et al, 2012) 54.…”

Genetic effect of an A/G polymorphism in the HSP70 gene on thermotolerance in chicken

“…Under conditions of thermostress, HSP70 synthesis is increased in order to protect the circulatory system from serious injury (Hartl, 1996;Gu et al, 2012). However, changes in gene expression for other reasons should also be considered, as they may not be associated with changes in the activity of gene products.…”