Figure 1.
Serum adiponectin levels in the three groups.
NC, normal control group; CIH, chronic intermittent hypoxia; CIH + Ad, chronic intermittent hypoxia and adiponectin supplement; **P<0.01 versus NC group; #P<0.05 versus CIH.
Table 1.
Echocardiographic data —5 weeks.
Figure 2.
A: Western blot analysis of GRP78 and CHOP in whole heart tissue homogenates. WB bands were normalized to β-actin. B: mRNA expressions of GRP78, CHOP in heart of three groups; PCR fluorescent signals for GRP78 and CHOP were standardized to PCR fluorescent signals obtained from an endogenous reference (β-actin). C: the densitometric evaluation of the independent western blot of GRP78; D: the densitometric evaluation of the independent western blot CHOP; *P<0.05 and **P<0.01 versus NC group; #p<0.05 and ##P<0.01 versus CIH group.
Figure 3.
IRE1 pathway activation in heart.
The protein levels of p-IRE1, IRE1, XBP-1 (s). Western blot band of p-IRE1 was normalized to IRE1. *P<0.05 versus NC group; #p<0.05 versus CIH.
Figure 4.
The protein levels of JNK1/2, P38 MAPK in heart.
The protein levels of p-JNK1/2, JNK1/2, p-P38 MAPK and P38 MAPK. Western blot bands of p-JNK1/2 and p-P38 MAPK were separately normalized to JNK1/2 and p-P38 MAPK. *P<0.05 versus NC group; #p<0.05 versus CIH group.
Figure 5.
PERK pathway activation in heart.
The protein levels of p-PERK, PERK, p-eIF2α, eIF2α. Western blot bands of p-PERK and p-eIF2α were separately normalized to PERK and eIF2α. *P<0.05 versus NC group; #p<0.05 versus CIH group.
Figure 6.
ATF6 pathway activation in heart.
The protein levels of pro-ATF6; *P<0.05 versus NC group; #p<0.05 versus CIH group.
Figure 7.
Detection of ROS generation of myocardium in three groups.
A: intracellular ROS generation detection in heart tissue. B: the values of fluorescence intensity in three groups. *P<0.05 versus NC group; #p<0.05 versus CIH group.
Figure 8.
The TUNEL staining of the heart.
Nuclei are shown in blue, and TUNEL staining is shown in green. The lower panels show the percentage of TUNEL-positive cell. *P<0.05 versus NC group; #p<0.05 versus CIH group.
Figure 9.
The protein levels of caspase-12, caspase-9, caspase-3.
Western blot bands of cleaved caspase-12, cleaved caspase-9 and cleaved caspase-3 were separately normalized to caspase-12, caspase-9 and caspase-3. *P<0.05 and **P<0.01 versus NC group; #p<0.05 and ##P<0.01 versus CIH group.
Figure 10.
Possible mechanisms of myocardium apoptosis induced by CIH.
(A) and protective roles of Ad (B). A: CIH can induce the ROS and then further causes ER stress represented by generation of misfold proteins, which combine Bip released from IRE1, PERK and ATF6. Upon Bip release, IRE1, PERK and ATF6 are activated. All of the three pathways finally upregulate the expression of CHOP, which may further trigger cell apoptosis. The IRE1 pathway also activates the JNK and P38 MAPK, which can trigger apoptosis. In addition, caspase-12 is activated during ER stress, which sequentially activates caspase-9 and/or caspase-3, leading to apoptosis. B: Through inhibition of ROS, Ad supplement may further suppress ERS and therefore the myocardial apoptosis may be reduced.