Recent studies show that combination of apoptosis and oxidative stress forms a “vicious circle” in the process of premature ovarian failure (POF). Pearl extract has a good effect for anti-oxidation and anti-aging in vitro and vivo and can be used to treat various aging diseases. However, reports about effect and mechanism of pearl on ovarian function of premature ovarian failure (POF)are limited. The effect and mechanism of pearl on ovarian function of rats with POF were evaluated using rats with premature ovarian failure induced by tripterygium glycosides. The estrous cycle, contents of serum reproductive hormones, tissue structure, oxidative stress level, autophagy and apoptotic protein expression, and MAPK signaling pathway of ovary were assessed to characterise pearl. Low, medium and high-dose pearl improved the estrous cycle in POF rats, and high-dose pearl was the best in terms of recovery effect; high-dose pearl significantly increased (P < 0.05) contents of E2, AMH and GSH, activities of SOD, CAT and GSH-PX and follicular development, while significantly decreased (P < 0.05)contents of FSH, LH and ROS and MDA in POF rats; low, medium and high-dose pearl notably reduced (P < 0.05) the apoptotic protein cleaved-caspase 3 and Bax expression, and MAPK signaling pathway of ERK1/2, p38 and JNK in POF rats, among which high-dose pearl behaved best. Medium and high-dose pearl apparently raised (P < 0.05)expressions of autophagy protein LC3II, Beclin-1 and p62 in POF rats. Therefore, pearl can effectively enhance ovarian function of POF rats. The optimal concentration was found to be 740 mg kg⁻¹ at a high dose. The mechanism may be related with the enhanced follicular development through improving granulosa cell autophagy and inhibiting granulosa cell apoptosis by inhibition of MAPK signaling pathway after scavenging excessive ROS. 1. Natural Products. Ovarian Cancer, Chinese Herbal Medicine, Traditional Medicine, Oxidative Stress, Antioxidant Studies, Rat, Autophagy.

Chronic obstructive pulmonary disease (COPD) is predicted to become the third leading cause of death around the world. The present study is designed to investigate whether hydrolyzed seawater pearl tablet (HSPT) has immunoregulatory effects on the Th1/Th2 functionality in cigarette smoke‐induced COPD model mice. The determination of the amino acid composition of HSPT was carried out by high‐performance liquid chromatography (HPLC) with precolumn phenylisothiocyanate (PITC) derivatization. COPD model mice were constructed by cigarette smoking (CS) treatment and HSPT was administered. HSPT inhibited the infiltration of inflammation in the airway of the lung, reduced influx of eosinophils (EOSs), lymphocytes (LYMs), neutrophils (NEUs), and macrophages (MACs) in the bronchoalveolar lavage fluid (BALF), decreased the levels of IFN‐γ, IL‐2, IL‐4, and IL‐10 in the serum and lung, and decreased the expression of aforementioned cytokines in the spleen and lung in CS‐treated mice. Besides, HSPT also had the ability to reduce the amount of CD3⁺CD4⁺ T cells and modulate the Th1/Th2 balance. Taken together, this study supports the consensus that CS is a critical factor to induce and aggravate COPD. HSPT could regulate the balance of Th1/Th2 in CS‐induced COPD model mice, indicating its effects on inhibiting the development of COPD.

Background: Ultraviolet (UV) is the main reason to cause photoaging skin which not only hinders beauty, brings the patients with psychological burden, but also pathologically leads to the occurrence of tumors in skin.Objective: This study goes into the inhibitory effect and mechanism of seawater pearl hydrolysate (SPH) to address human skin keratinocytes photoaging induced by UVB.Methods: The photoaging model of Hacat cell was constructed by UVB irradiation, the levels of oxidative stress, apoptosis, aging, autophagy and autophagy‐related protein and signal pathway expression were assessed to characterize the inhibitory effect and mechanism of SPH on photoaging Hacat cell.Results: Seawater pearl hydrolysate significantly accelerated (p < 0.05) the activities of superoxide dismutase, catalase, and glutathione peroxidase, and markedly reduced (p < 0.05) the contents of reactive oxygen species (ROS), malondialdehyde, protein carbonyl compound and nitrosylated tyrosine protein, aging level, apoptosis rate in Hacat cell induced by 200 mJ cm⁻² UVB after 24 and 48 h of culture; high dose SPH significantly raised (p < 0.05) relative expression level of p‐Akt, p‐mTOR proteins, and markedly decreased (p < 0.05) relative expression level of LC3II protein, p‐AMPK, and autophagy level in Hacat cell induced by 200 mJ cm⁻² UVB, or in combination with the intervention of PI3K inhibitor or AMPK overexpression after 48 h of culture.Conclusion: Seawater pearl hydrolysate can effectively inhibit 200 mJ cm⁻² UVB‐induced photoaging of Hacat cells. The mechanism indicates removing the excessive ROS through increasing the antioxidation of photoaging Hacat cells. Once redundant ROS is eliminated, SPH works to reduce AMPK, increase PI3K‐Akt pathway expression, activate mTOR pathway to lowdown autophagy level, and as a result, inhibit apoptosis and aging in photoaging Hacat cells.

The objective of this study was to investigate the therapeutic effect of seawater pearl powder (SPP) on ultraviolet (UV) irradiation-induced photoaging in mouse skin. The protein and trace elements in SPP were detected by liquid chromatography-mass spectrometry, atomic fluorescence spectrometry, and inductively coupled plasma-atomic emission spectrometry. The effect of SPP on treating skin damage resulting from UV-induced photoaging was observed by gross physical appearance and histopathological analysis. Oxidative stress and melanin synthesis were analyzed using biochemical method. Western blotting was applied to analyze the phosphorylation and expression levels of matrix metalloproteinase-1 (MMP-1), collagen I, and proteins involved in the mitogen-activated protein kinase (MAPK) signaling pathways (p38, ERK, and JNK). The results show that SPP has a significant therapeutic effect on UV-induced photoaging of skin and improves and restores appearance and tissue structure of mouse skin. The major mechanism may be related to reduction of expression level of MMP-1 and enhancement of collagen I production via inhibition of MAPK signaling pathway after scavenging of excess reactive oxygen species (ROS) in the UV-induced photoaged skin of mice. Meanwhile, it may also be involved in reducing melanin content by inhibiting tyrosinase activity after scavenging excess ROS in the UV-induced photoaged skin of mice. Therefore, SPP could be a good substance to treat photoaging skin. Taking cost-effectiveness and efficacy into consideration, the optimal concentration of SPP for treating photoaging skin could be 100 mg/g.