This study aimed to investigate the effect of quercetin on apoptotic cell death induced by ischemia-reperfusion (I/R) injury in the rat retina. Twenty-four rats were divided into four equal groups: control, ischemic, solvent, and quercetin. I/R injury was achieved by elevating the intraocular pressure above the perfusion pressure. Intraperitoneal injections of 20 mg/kg of quercetin and dimethyl sulfoxide (DMSO) were performed in the quercetin and solvent groups, respectively, immediately prior to I/R injury, and the researchers allowed for the retinas to be reperfused. Forty-eight hours after injury, the thicknesses of the retinal ganglion cell layer (RGCL), inner nuclear layer (INL), inner plexiform layer (IPL), outer plexiform layer (OPL), and outer nuclear layer (ONL) were measured in all groups. Moreover, the numbers of terminal deoxynucleotidyl transferase dUTP nick-end-labeled [TUNEL (+)] cells and caspase-3 (+) cells in both INL and ONL were evaluated in all groups. The administration of quercetin was found to reduce the thinning of all retinal layers. The mean thickness of INL in the quercetin and ischemic groups was 21 ± 5.6 µm and 16 ± 6.4 µm, respectively (P<0.05). Similarly, the mean thickness of ONL in the quercetin and ischemic groups was 50 ± 12.8 µm and 40 ± 8.7 µm, respectively (P<0.05). The antiapoptotic effect of quercetin in terms of reducing the numbers of both TUNEL (+) cells and caspase-3 (+) cells was significant in INL. The mean number of TUNEL (+) cells in INL in the ischemic and quercetin groups was 476.8 ± 45.6/mm2 and 238.72 ± 251/mm2, respectively (P<0.005). The mean number of caspase-3 (+) cells in INL of ischemic and quercetin groups was 633.6 ± 38.7/mm2 and 342.4 ± 36.1/mm2, respectively (P<0.001). The use of quercetin may be beneficial in the treatment of retinal I/R injury because of its antiapoptotic effect on the retinal layers, particularly in INL.

The trinitrobenzene sulfonic acid (TNBS) induced colitis model is used to investigate the pathogenesis of ulcerative colitis. Colon inflammation and apoptosis are associated with tissue damage in ulcerative colitis. Hesperetin is a natural flavonoid that exhibits antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hesperetin on tumor necrosis factor-alpha (TNF-α), protein tyrosine phosphatase, receptor type C (CD45), caspase-3 and Bax expressions in TNBS in induced colitis model in rats. Male rats were divided into three groups: control group treated with 1 ml physiological saline, colitis group, and colitis + hesperetin group treated with TNBS and hesperetin. Hesperetin treatment was applied for 10 days starting 3 days prior to colitis induction. At the end of the experiment, TNF-α, CD45, caspase-3 and Bax expressions in colon tissue were determined using indirect immunohistochemistry. Increased immunoreactivity of both inflammation markers, TNF-α, CD45, and apoptotic markers, caspase-3 and Bax, was detected in the colitis group. Hesperetin treatment effected significant reduction of all parameters. Hesperetin treatment prevents colon damage owing to its anti-inflammatory and anti-apoptotic effects.

We investigated the gastroprotective effect of apricot kernel oil on ethanol induced gastric ulcer in rats. Male Wistar albino rats were divided into control, ethanol and apricot kernel oil + ethanol groups. The fatty acid composition of apricot kernel oil was determined using GC-MS. A gastric ulcer index was defined as the area percentage of the gastric mucosa consisting of ulcerated tissue. Gastric tissue was investigated by TUNEL staining for apoptosis, immunohistochemical iNOS staining, measurement of gastric IL-10 and IL-6 expression by ELISA and assays of catalase, malondialdehyde and superoxide dismutase. The ethanol group exhibited a higher gastric ulcer score, increased IL-6 level, increased number of inducible nitric oxide synthase-positive and TUNEL positive cells, and a higher MDA level compared to the control group. The apricot kernel oil + ethanol group exhibited significantly fewer gastric lesions compared to the ethanol group. Apricot kernel oil protects rat gastric mucosa against ethanol induced injury by its anti-inflammatory, anti-oxidative and anti-apoptotic effects, and might be useful for reducing the severity of gastric ulcers.

We investigated the effects of caffeic acid phenethyl ester (CAPE) on cardiac damage after blunt chest injury. Forty male adult Wistar albino rats were divided into four groups; control, cardiac contusion, cardiac contusion + CAPE, and CAPE. CAPE, 10 mmol/kg, was administered intraperitoneally for 7 days following cardiac contusion. Heart tissue and blood were obtained at the end of the experimental period. Cardiac histopathology was determined using hematoxylin & eosin (H & E) staining. Expression of tumor necrosis factor-alpha (TNF-α) in cardiomyocytes was determined using immunohistochemistry. Cardiac apoptosis was determined using the TUNEL method. Serum creatine kinase (CK), creatine kinase-muscle/brain (CK-MB) and lactate dehydrogenase (LDH) levels were determined using spectrophotometric methods. The serum cardiac troponin I (C-TI) level was measured using the ELISA method. Myofibril loss was detected in the cardiomyocytes of the cardiac contusion group. Increased apoptosis and TNF-α expression were observed in the cardiac contusion group compared to the control group. Increased CK, CK-MB, LDH and C-TI levels were found in the cardiac contusion group. We found that CAPE administration improved myocardial function. Compared to the cardiac contusion group, CK, CK-MB, LDH and C-TI levels decreased significantly in the cardiac contusion + CAPE group. Administration of CAPE significantly inhibited apoptosis and cardiac TNF-α expression. Our findings demonstrate the therapeutic effects of CAPE for cardiac contusion damage after blunt chest trauma.