Impact of Moriamin Forte on Testicular and Epididymal Damage in Rats with Oligoasthenospermia

To investigate the effect and mechanism of action of Moriamin Forte (MF) on oligoasthenospermia (OA) in rats exposed to multiglycosides of Tripterygium wilfordii (GTW), forty male Sprague Dawley rats were randomly divided into four groups. Rats in the control group were treated with 0.5% sodium carboxymethyl cellulose. The remaining rats were administered GTW (30 mg/kg/d) for 40 d to establish an OA model. Concurrently, the groups were treated with normal saline and low-dose (100 mg/kg/d) and high-dose (200 mg/kg/d) MF, respectively. After treatment, the number and motility of sperm cells were examined. Testicular and epididymal histomorphology changes were observed. Antioxidant indicators (SOD, CAT, MDA, TAC, and Nrf2) in testicular and epididymal tissues were detected. Apoptotic and antiapoptotic indicators (Bax and Bcl2 expression) in the testicular tissue were measured by immunohistochemistry. GTW decreased sperm count and motility, damaged testicular and epididymis tissues, impaired antioxidase activity, and increased tissue MDA levels. Meanwhile, GTW upregulated the expression of Bax and downregulated the expression of Bcl2. Western blot analysis demonstrated a decrease in the Nrf2 expression in the model group. Treatment with MF improved sperm count and motility, as well as inhibited the rate of apoptosis in the rat reproductive system. Moreover, MF improved the activity of antioxidants and increased the relative expression of the antioxidant pathway-related protein Nrf2. In conclusion, MF may reverse the GTW-induced OA by modulating the expression of apoptotic and antioxidant pathway-related proteins. This study may provide a pharmacological foundation for the use of MF in OA treatment.

SGLT1 knockdown prevents glucose fluctuation-induced apoptosis of cardiomyocytes through attenuating oxidative stress and mitochondrial dysfunction

Blood glucose fluctuation has been validated to be more detrimental than constant high glucose in the development of cardiovascular complications of diabetes mellitus (DM). Sodium‑glucose cotransporter 2 (SGLT2) inhibitors have been developed as antidiabetic drugs with cardiovascular benefits. However, whether inhibition of SGLT1 protects the diabetic heart remains to be elucidated. The present study investigated the role of SGLT1 in rat H9c2 cardiomyocytes subjected to glucose fluctuation and the underlying mechanisms. The results indicated that SGLT1 knockdown was able to restore cell proliferation and suppress cytotoxicity induced by glucose fluctuation. Glucose fluctuation induced oxidative stress in H9c2 cells, while these changes were reversed effectively by SGLT1 knockdown, as manifested by reduction of intracellular reactive oxygen species and increased antioxidase activity. Further study demonstrated that SGLT1 knockdown attenuated mitochondrial dysfunction in H9c2 cells exposed to glucose fluctuation, including restoration of mitochondrial membrane potential and promotion of mitochondrial fusion. In addition, SGLT1 knockdown downregulated Bax expression, upregulated Bcl-2 expression, and reduced caspase-3 activation in glucose fluctuation-induced H9c2 cells. Taken together, our study reveals that SGLT1 knockdown ameliorates glucose fluctuation-induced cardiomyocyte apoptosis, which might be ascribed to regulation of oxidative stress and mitochondrial dysfunction.

Response of Photosynthetic Performance to Drought Duration and Re-Watering in Maize

The drought tolerance and capacity to recover after drought are important for plant growth and yield. In this study, two maize lines with different drought resistance were used to investigate the effects of different drought durations and subsequent re-watering on photosynthetic capacity, electron transfer and energy distribution, and antioxidative defense mechanisms of maize. Under short drought, maize plants decreased stomatal conductance and photosynthetic electron transport rate, and increased NPQ (Non-photochemical quenching) to dissipate excess excitation energy in time and protect the photosynthetic apparatus. With the increased drought duration, NPQ, antioxidase activity, PItotal (total performance index), ∆I/Io, ψEo (quantum yield for electron transport), φEo (efficiency/probability that an electron moves further than QA−), δRo (efficiency/probability with which an electron from the intersystem electron carriers is transferred to reduce end electron acceptors at the PSI acceptor side) and φRo (the quantum yield for the reduction of the end electron acceptors at the PSI acceptor side) were significantly reduced, while Y(NO) (quantum yield of nonregulated energy dissipation) and MDA (malondialdehyde) began to quickly increase. The photosynthetic rate and capacity of photosynthetic electron transport could not recover to the level of the plants subjected to normal water status after re-watering. These findings indicated that long drought damaged the PSI (photosystem I) and PSII (photosystem II) reaction center and decreased the electron transfer efficiency, and this damage could not be recovered by re-watering. Different drought resistance and recovery levels of photosynthetic performance were achieved by different maize lines. Compared with D340, D1798Z had higher NPQ and antioxidase activity, which was able to maintain functionality for longer in response to progressive drought, and it could also recover at more severe drought after re-watering, which indicated its higher tolerance to drought. It was concluded that the capacity of the energy dissipation and antioxidant enzyme system is crucial to mitigate the effects caused by drought, and the capacity to recover after re-watering was dependent on the severity and persistence of drought, adaptability, and recovery differences of the maize lines. The results provide a profound insight to understand the maize functional traits’ responses to drought stresses and re-watering.

The Effects of Maternal Obesity on Porcine Placental Efficiency and Proteome

Maternal obesity is associated with impaired maternal metabolism and affects the developmental programming of the fetus. The placenta is dysfunctional when exposed to an obese intrauterine environment and can transduce and mediate detrimental maternal impacts to the fetus through mechanisms that remain largely unknown. The main objective of this study was to investigate the effects of maternal obesity on the porcine placental proteome and to analyze the deregulated proteins and potential pathways predicted to be disturbed in obese placentas, using sows with high backfat as a model of obese pregnancy. The sows were divided into two groups based on their backfat thickness: normal backfat (NBF, 17–22 mm; n = 30) and high backfat (HBF, ≥23 mm; n = 30) as the maternal obesity group. The placental tissues used for the proteomic and biochemical analyses were obtained through vaginal delivery, and the maternal blood samples used to determine the metabolic parameters were collected at day 107 of pregnancy. Our study demonstrated that HBF sows had significantly decreased placental efficiency, increased plasma-free fatty acids and triglyceride levels, and increased proinflammatory cytokines plasma levels (p < 0.05). HBF placentas had significantly higher malondialdehyde level, lower total antioxidant capacity and antioxidase activity, increased triglyceride content and enhanced proinflammatory tumor necrosis factor- α (TNF-α) and interleukin-6 (IL-6) contents (p < 0.05). Among the 4652 proteins identified using the proteomic method, 343 were quantified as differentially abundant proteins, which were involved in many vital biological processes. Based on our bioinformatic and placental biochemical analyses, we concluded that maternal obesity is associated with abnormal carbohydrate and lipid metabolism, mitochondrial dysfunction, decreased steroid hormone biosynthesis, and increased oxidative stress and inflammation in the placenta. The results of this study are undoubtedly valuable to other researchers.

Short-term physiological responses to drought stress in seedling of tropical and temperate maize (Zea mays L.) cultivars

Understanding of the response of tropical and temperate maize (Zea mays L.) to drought is the first step for tolerant temperate maize improvement. Eight maize hybrids were used to investigate physiology responses under drought stress, four of them were tropical maize and the others were temperate maize. Results showed that there were different drought tolerances but similar trends in both tropical maize and temperate maize. Gas exchange parameters revealed different strategies of maize under the stress. In our study, most of the temperate hybrids maintained open stomata to keep a higher photosynthesis rate at the beginning of stress, while the other hybrids decreased stomatal conductance. Compared to temperate maize, the tropical maize had higher antioxidase activity and greater physiological parameter variation among hybrids. KS5731 and ZD309 had stronger drought resistance among tropical and temperate maize hybrids separately. Tolerant hybrids maintained active photosynthesis, have higher osmotic adjustment ability and antioxidase activities but lower malonaldehyde content than the sensitive ones. Our results led to a better understanding of the physiological responses of tropical and temperate maize plants to drought stress and may provide an insight of breeding for drought resistance in maize.

The Protective Effects of Sika Deer Antler Protein on Cisplatin-Induced Nephrotoxicity

Background/Aims: This study measured the effect of Sika deer (Cervus nippon Temminck) antler protein (SDAPR), glycoproteins (SDAG), and polysaccharides (SDAPO) on cisplatin-induced cytotoxicity in HEK 293 cells, and investigated the effect of SDAPR against cisplatin-induced nephrotoxicity in mice. Methods: Cell viability was measured by MTT assay. ICR mice were randomly divided into five groups: control, cisplatin with vehicle, and cisplatin with SDAPR at three concentrations: 5, 10, or 20 mg/kg, p.o., 10 d. Cisplatin was injected on 7th day (25 mg/kg, i.p.). Renal function, oxidative stress, levels of inflammatory factors, and expression of apoptosis-related proteins were measured in vivo. Renal tissues were stained with TUNEL and H&E to observe renal cell apoptosis and pathological changes. Results: Pretreatment with SDAPR (125-2000 µg/mL) significantly improved cell viability, with an EC50 of approximately 1000 µg/mL. SDAPR also ameliorated cisplatin-induced histopatholo- gic changes, and decreased blood urea nitrogen (BUN) and creatinine (Cr) (P < 0.05). Western blotting analysis showed SDAPR clearly decreased expression levels of cleaved-caspase-3 and Bax, and increased the expression level of Bcl-2 (P < 0.01). Additionally, SDAPR markedly regulated oxidative stress markers and inflammatory cytokines (P<0.05). TUNEL staining showed decreased apoptosis after SDAPR treatment (P < 0.01). Conclusions: These results indicate that SDAPR can be an effective dietary supplement, to relieve cisplatin-induced nephrotoxicity by improved antioxidase activity, suppressed inflammation, and inhibited apoptosis in vivo.

Antioxidant and Hepatoprotective Effect of Swertiamarin on Carbon Tetrachloride-Induced Hepatotoxicity via the Nrf2/HO-1 Pathway

Background/Aims: Swertiamarin (STM), the main bioactive component in Swertia mussotii Franch (Gentianaceae), has been shown to exert hepatoprotective effects on experimental liver injury. However, the effects and exact mechanisms of STM on carbon tetrachloride (CCl4) causing hepatotoxicity are still unknown. This study investigated the potential protective effects and mechanisms of STM on CCl4-induced liver injury in rats. Methods: Adult male Sprague-Dawley (SD) rats were exposed to CCl4 with or without STM co-administration for consecutive eight weeks. Results: STM significantly ameliorated CCl4-induced increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels and histopathological changes in the liver. Hepatic oxidative stress was repressed by STM, as evidenced by the decrease in malondialdehyde (MDA), with concomitant increase in antioxidase activity (e.g. superoxide dismutase (SOD); glutathione peroxidase (GPx)), glutathione (GSH) level. STM also obviously attenuated inflammatory response in CCl4-lesioned livers as evidenced by the decrease in inflammatory cytokines/ chemokines (e.g. inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β)). Additionally, STM significantly induced the expression of CYPs, efflux transporters and PDZK1 as compared with the CCl4 group. Moreover, co-administration of STM with CCl4 remarkably up-regulated the expression of Nrf2, HO-1 and NQO1 compared with the CCl4 group. Conclusions: The present study demonstrates that STM exerts a protective effect against CCl4-induced liver injury and inflammation with its antioxidant effects and induction of hepatic detoxification enzymes and efflux transporters expression, at least in part, via the Nrf2/HO-1 pathway in rats.